The alterations in the miRNA expression profile play a crucial role in the onset and progression of various human malignancies. Consequently, the development of sensitive, specific, and precise methods for miRNA detection represents a promising tool for diagnosing and treating of cancers. In this study, we propose a highly sensitive detection strategy for tumor-associated miRNAs utilizing a three-way junction (TWJ) mediated strand displacement amplification (SDA) cascade coupled with catalyzed hairpin assembly (CHA). This approach enables the accurate discrimination of miRNAs from other RNA molecules through target recognition and proximity effects facilitated by the TWJ structure, which subsequently triggers SDA for initial amplification. In addition, the CHA underwent a second round of amplification, which ultimately enabled the successful detection of low-abundance miRNA. Leveraging the signal amplification method of dual isothermal amplification, this strategy demonstrates excellent linearity from 1 pM to 10 nM, with a detection limit of 0.24 pM. Notably, this approach holds significant potential for practical applications in real samples, offering a novel method to investigate the expression profiles of various miRNAs in different tumor cells and to elucidate the underlying mechanisms of miRNAs in tumorigenesis and progression.

Cancer progression is a multifaceted process influenced by complex interactions within the tumor microenvironment (TME). Central to these dynamics are Vascular Endothelial Growth Factor (VEGF) signalling and microRNA (miRNA) modulation, both of which play critical roles in tumor growth and angiogenesis. VEGF is essential for promoting blood vessel formation; however, its splice variant, VEGF165b, acts as an anti-angiogenic factor, presenting a paradox challenging conventional cancer therapies. Meanwhile, miRNAs regulate gene expression that significantly impacts tumor behaviour by targeting various mRNAs involved in signalling pathways. The interplay between VEGF and miRNAs opens new avenues for targeted therapies designed to disrupt the networks supporting tumor growth. Additionally, the concept of exploiting the unique properties of VEGF splice variants is being explored to develop novel treatments that enhance anti-angiogenic effects while minimizing side effects. Understanding this is crucial for advancing personalized therapies that can effectively address the challenges posed by tumor adaptability and resistance mechanisms.

miR-135b, a microRNA, is consistently up-regulated in various cancer tissues and cells, promoting cancer progression. By inhibiting one or more target genes, miR-135b regulates phenotypes such as cancer growth, apoptosis, migration, invasion, drug resistance, and angiogenesis, establishing it as a critical driver of cancer progression. Additionally, miR-135b is regulated by various oncogenes and therapeutic drugs, highlighting its complexity and therapeutic potential. Significant progress has been made in understanding miR-135b's impact on cancer cell behavior, establishing it as a promising biomarker for cancer diagnosis and prognosis, as well as a potential target for future cancer therapies. However, despite the extensive research on this topic, there has been no comprehensive review summarizing its role and mechanisms across different cancer types. This review aims to provide a detailed overview of the biological characteristics of miR-135b, its regulatory targets, upstream signaling pathways, and its therapeutic potential, including its influence on cancer chemoresistance. The review also addresses key controversies surrounding miR-135b in cancer research, aiming to deepen the understanding of its role, promote the transformation of its clinical application, and provide a theoretical foundation for developing more effective cancer treatment strategies.

Small non-coding RNAs (e.g., siRNA, miRNA) are involved in a variety of melanocyte-associated skin conditions and act as drivers for alterations in gene expression within melanocytes. These molecular changes can potentially affect the cellular stability of melanocytes and promote their oncogenic transformation. Thus, small RNAs can be considered as therapeutic targets for these conditions, however, their transdermal delivery to the melanocytes through the epidermal barrier is challenging. We synthesized and extensively evaluated ultradeformable cationic liposome (UCLs) carriers complexed with synthetic microRNAs (miR211-5p; UCL-211) for transdermal delivery to melanocytes. UCL-211 complexes were characterized for their physicochemical properties, encapsulation efficiency, and deformability, which revealed a significant advantage over conventional liposomal carriers. Increased expression of miR211-5p stabilizes melanocytic nevi and keeps them in a growth-arrested state. We did a comprehensive assessment of cellular delivery, and biological activity of the miR211-5p carried by UCL-211 in vitro and their permeation through the epidermis of intact skin using ex vivo human skin tissue explants. We also demonstrated, in vivo, that transdermal delivery of miR211-5p by topical application of UCL-211 stabilized BRAFV600E+ nevi melanocytes in a benign nevi state.

Gastric cancer (GC)，the fourth leading cause of cancer-related deaths globally and thus early detection, is considered critical for diagnosis and treatment of this disease. It is well known that measurement of microRNA (miRNA) may serve as diagnostic and prognostic biomarker for GC. The aim of this study was to determine whether miR-30c was present in patients with gastric cancer and to correlate relative expression with patient survival. A total of 162 GC patients and 150 healthy controls were recruited. miR-30c levels were quantified in serum using quantitative real-time PCR(QRT-PCR). The sensitivity and specificity of circulating miR-30c was compared to carbohydrate antigen (CA) CA72-4, CA19-9, and carcinoembryonic antigen (CEA), 3 known markers associated with GC. QRT-PCR demonstrated downregulation of gene expression of miR-30c in GC patients. Downregulation of miR-30c gene expression was significantly correlated with stage of cancer, lymphatic metastasis, and distal metastasis. The sensitivity to detect GC of miR-30c, CA72-4, CA19-9, and CEA in serum of GC was 80%, 43%, 21%, and 42%, respectively, while specificity was 89%, 57%, 30%, and 78% respectively. Kaplan-Meier survival analysis showed that the presence of low gene expression of miR-30c was effective in predicting poor prognosis in GC patients. Our data suggest that circulating serum miR-30c concentrations may serve as a reliable biomarker for GC occurrence. (212words).

Cancer metastasis is a complicated biological process that critically affects cancer progression, patient outcomes, and treatment plans. A significant step in metastasis is the formation of a pre-metastatic niche (PMN). A small subset of cells within tumors, known as cancer stem cells (CSCs), possess unique characteristics including, differentiation into different cell types within the tumor, self-renewal, and resistance to conventional therapies, that enable them to initiate tumors and drive metastasis. PMN plays an important role in preparing secondary organs for the arrival and proliferation of CSCs, thereby facilitating metastasis. CSC-derived exosomes are crucial components in the complex interplay between CSCs and the tumor microenvironment. These exosomes function as transporters of various substances that can promote cancer progression, metastasis, and modulation of pre-metastatic environments by delivering microRNA (miRNA, miR) cargo. This review aims to illustrate how exosomal miRNAs (exo-miRs) secreted by CSCs can predispose PMN and promote angiogenesis and metastasis.

As living standards elevate, cancers are appearing in growing numbers among younger individuals globally and these risks escalate with advancing years. One of the reasons is that instability in the cancer genome reduces the effectiveness of conventional drug treatments and chemotherapy, compared with more targeted therapies. Previous research has discovered non-coding RNAs' crucial role in shaping genetic networks involved in cancer cell growth and invasion through their influence on messenger RNA production or protein binding. Additionally, the interaction between non-coding RNAs and oxidative stress, a crucial process in cancer advancement, cannot be overlooked. Essentially, oxidative stress results from the negative effects of radicals within the body and ties directly to cancer gene expression and signaling. Therefore, this review focuses on the mechanism between non-coding RNAs and oxidative stress in cancer progression, which is conducive to finding new cancer treatment strategies.

Chronic lymphocytic leukemia (CLL) is a malignant lymphoproliferative disorder. Long non-coding RNAs (lncRNAs) have been implicated in various regulatory processes and cancer development. Among these, lncRNA tumor suppressor candidate 7 (TUSC7) has been identified as a tumor suppressor gene. We herein measured TUSC7 expression using RT-qPCR and investigated its biological role in CLL through gain-of-function experiments. Our results revealed that TUSC7 expression was significantly lower in CLL patients compared to healthy controls, and its downregulation was associated with poor prognosis. Meanwhile, TUSC7 overexpression inhibited cell proliferation while promoting cell apoptosis. Mechanistically, TUSC7 interacted with miR-211-5p, thereby regulating the downstream target gene, solute carrier family 37 member 3 (SLC37A3). Further rescue experiments demonstrated that silencing SLC37A3 or upregulating miR-211-5p reversed the effects of TUSC7 elevation on cell proliferation and apoptosis. In conclusion, our findings suggest that TUSC7 regulates cell proliferation in CLL through the miR-211-5p/SLC37A3 axis.

Anaplastic thyroid cancer (ATC) is a rare lethal human malignancy with a poor prognosis. Multimodality treatment, including radiotherapy, is recommended to improve local control and survival. Valproic acid (VA) is a clinically available anticonvulsant and histone deacetylase inhibitor with a well-documented side effect profile. Furthermore, VA radiosensitizes various cancer cells, including thyroid cancer. MicroRNAs (miRs) are deregulated in several cancers and may modulate radiation response. Therefore, the aim of this study was to analyze the effect of VA combined with gamma radiation in radioresistant ATC cells at the expression level of miRs.

ATC cells (8505c and KTC-2) were VA-treated and gamma-irradiated (2 Gy). The expression profile of miRs in 8505c was evaluated by microarray analysis 4 h after irradiation. Selected miRs were validated by RT-qPCR in both types of ATC cells.

We observed that after combined VA and gamma irradiation treatment, 8505c cells showed 109 differentially expressed miRs as compared to irradiated cells alone. These miRs exhibited a radiosensitization profile highlighted by upregulation of hsa-miR-26a-5p, which is usually downregulated in aggressive thyroid cancers. Moreover, hsa-miR-27a-3p and hsa-miR-486-5p, which are often deregulated in thyroid neoplasms, were downregulated after irradiation and VA treatment, respectively. The expression level of these three miRs was validated in 8505c and KTC-2 cells after treatments.

The regulated miRs by VA and gamma irradiation reveal a novel miR expression profile with potential to be further studied in the radio-induced response and radiosensitization of ATC cells.

The interaction between tumor-derived exosomes and stroma plays a crucial role in tumor progression. However, the mechanisms through which tumor cells influence stromal changes are not yet fully understood. In our study, through single-cell sequencing analysis of clear cell renal cell carcinoma tissues at varying stages of progression, we determined that the proportion of cancer-associated fibroblasts (CAFs) in advanced renal cell carcinoma tissues was notably higher compared to localized renal cell carcinoma tissues. Comparison of transcriptome sequencing and energy metabolism tests between CAFs primarily isolated from advanced renal cell carcinoma tissues and normal fibroblasts (NFs) revealed the occurrence of the Warburg effect during the fibroblast activation process. Additionally, we observed an increase in glucose transporter GLUT1 expression, total reactive oxygen species (ROS) levels, lactic acid production, and subsequent excretion of excess lactic acid through monocarboxylate transporter-4 (MCT4) in CAFs. Interestingly, renal cancer cells were found to uptake lactic acid via MCT1 upon interaction with CAFs, thereby enhancing their malignant phenotypes. Furthermore, the down-regulation of PANK3 induced by exosomes derived from renal cancer cells was identified as a crucial step in fibroblast activation. These findings indicate that exosomes play a role in facilitating intercellular communication between renal cancer cells and fibroblasts. Targeting this communication pathway could potentially offer new strategies for the prevention and treatment of advanced renal cell carcinoma.

The integration of nanomaterials with DNA-based systems has emerged as a transformative approach in biosensing and therapeutic applications. Unique features of DNA, like its programmability and specificity, complement the diverse functions of nanomaterials, leading to the creation of advanced systems for detecting biomarkers and delivering treatments. Here, we review the developments in DNA-nanomaterial conjugates, emphasizing their enhanced functionalities and potential across various biomedical applications. We first discuss the methodologies for synthesizing these conjugates, distinguishing between covalent and non-covalent interactions. We then categorize DNA-nanomaterials conjugates based on the properties of the DNA and nanomaterials involved, respectively. DNA probes are classified by their application into biosensing or therapeutic uses, and, several nanomaterials are highlighted by their recent progress in living biological. Finally, we discuss the current challenges and future prospects in this field, anticipating that significant progress in DNA-nanomaterial conjugates will greatly enhance precision medicine.

This study aimed to investigate the effect of miR-325 on KIF20B expression and its role in the invasion and proliferation of colorectal cancer cells.

Colorectal cancer HCT116 cells were cultured and transfected with a miR-325 inhibitor. KIF20B expression was assessed using quantitative polymerase chain reaction (qPCR) and western blotting. Cell proliferation was assessed with the Cell Counting Kit-8 (CCK8) assay, while invasion was evaluated using Transwell and scratch wound healing assays. The expression levels of the invasion-related proteins Matrix Metalloproteinase-2 (MMP-2) and MMP-9 were also analyzed.

The q-PCR and western blot results demonstrated that KIF20B expression was significantly reduced by miR-325 inhibition. The CCK8 assay revealed that miR-325 inhibition decreased cell proliferation. Furthermore, Transwell and Scratch Wound Healing assays showed that miR-325 inhibition suppressed the invasive capacity of colorectal cancer cells. The inhibition of miR-325 also led to decreased expression levels of MMP-2 and MMP-9.

miR-325 inhibition effectively suppresses KIF20B expression, reducing the invasion and proliferation of colorectal cancer cells, suggesting miR-325 as a potential therapeutic target.

The association between microRNA 17-92 cluster host gene (MIR17HG) polymorphisms and the risk of cancer has been evaluated in studies, here, we attempted to elucidate the relationship between 6 single nucleotide polymorphisms (SNPs) of MIR17HG (rs17735387 G > A, rs7336610 C > T, rs1428 C > A, rs7318578 A > C, rs72640334 C > A, and rs75267932 A > G), 3 SNPs in the promoter of MIR17HG (rs9588884 C > G, rs982873 T > C, and rs1813389 A > G) and susceptibility to cancer in Chinese Han population.

Systematic literature research from databases were performed with strict eligibility criteria to include the relevant studies for this meta-analysis. Association between the SNPs of MIR17HG and cancer risk was estimated by pooling the odds ratios (ORs) with 95% confidence interval (95% CI) in five genetic models (allelic model, dominant model, recessive model, homozygous model, and heterozygous model).

The pooled meta-analysis showed that there was no significant association between rs17735387 G > A, rs7336610 C > T, rs1428 C > A, rs7318578 A > C, rs72640334 C > A, and rs75267932 A > G and cancer risk in Chinese Han population. However, for the SNPs in the promoter of MIR17HG, rs9588884 C > G and rs982873 T > C could decrease cancer risk in most genetic models, but not rs1813389 A > G.

This present meta-analysis identified 2 SNPs in the promoter of MIR17HG (rs9588884 C > G and rs982873 T > C) may be protective factors against cancer in Chinese Han population.

A self-driven and self-catalytic (SDSC) tripedal DNA nanomachine was developed for microRNA-21 (miR-21) detection. The microRNA could open one arm of tripedal DNA nanomachine to form DNAzyme with a nearby arm through the proximity effect. After DNAzyme's cleavage, the exposed DNA arm region competed with the third arm and produced a DNA segment (sequence Q). The released sequence Q initiated the next SDSC cycle of tripedal DNA nanomachine. In the special DNA nanomachines design, the components with close spatial localization were constructed on a single nanostructure, which significantly increased local reactant concentrations and reaction rates. A dynamic correlation was obtained from 10 pM to 50 nM between fluorescence signal and miR-21 concentration. The effective concentration of reactant greatly increased, compared with the free diffusible reactants. Consequently, the incubation time was significantly shorted to 35 min. This strategy showed a promising potential in miRNA detection and disease diagnosis.

A product-induced catalytic amplification (PICA) strategy had been developed for miRNA-21 detection based on DNA tetrahedron module (DTM). The produced DNA fragment could open hairpin structure and increase the concentration of catalyst, accelerating the circular cleavage reaction on DTM by DNAzyme cleavage. The continuously cleavage of DNAzyme on DTM resulted the greatly enhancement of signal. A favorable linear range was achieved from 20 pM to 5 nM with a limit of detection of 7 pM. Furthermore, through the implementation of the PICA strategy, the overall reaction time experienced a noticeable decrease to 30 min. The assessments of the amplification rate and kinetic constant of the PICA strategy were also conducted. These results highlighted the promising potential of the PICA strategy for practical utilization in serum samples.

Colorectal cancer (CRC) is a leading cause of death worldwide due to its aggressive nature and drug resistance, which limit traditional treatment effectiveness. Recent studies highlight the role of microRNAs (miRNAs) in tumorigenesis, metastasis, and chemotherapy resistance, with miRNA-155 emerging as a key player in CRC. miRNA-155 exerts dual effects, inducing drug resistance while serving as a potential therapeutic target. It regulates a wide array of mRNA transcripts associated with apoptosis, cell cycle regulation, and DNA repair, impacting various cellular pathways. Overexpression of miRNA-155 is linked to resistance against multiple chemotherapeutic drugs, promoting tumor cell survival, proliferation, and the epithelial-mesenchymal transition (EMT) process by repressing tumor suppressors and activating oncogenes. Additionally, miRNA-155 holds promise as a diagnostic and prognostic marker due to its association with CRC patient survival rates. However, its regulatory mechanisms across CRC subtypes remain unclear. This study provides insights into miRNA-155's role in CRC, focusing on its involvement in therapeutic resistance and potential as a therapeutic target. We also explore its significance as a prognostic biomarker and emphasize its therapeutic applications based on evidence from human, in vivo, in vitro, and clinical studies.

Less than 5% of the DNA sequence encodes for proteins, and the remainder encodes for non-coding RNAs (ncRNAs). Among the members of the ncRNA family, microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) play a pivotal role in the insurgence and progression of several cancers, including leukemia. Thought to have different molecular mechanisms, both miRNAs and lncRNAs act as epigenetic factors modulating gene expression and influencing hematopoietic differentiation, proliferation and immune system function. Here, we discuss the most recent findings on the main molecular mechanisms by which miRNAs and lncRNAs are involved in the pathogenesis and progression of pediatric T acute lymphoblastic leukemia (T-ALL), pointing out their potential utility as therapeutic targets and as biomarkers for early diagnosis, risk stratification and prognosis. miRNAs are involved in the pathogenesis of T-ALL, acting both as tumor suppressors and as oncomiRs. By contrast, to the best of our knowledge, the literature highlights lncRNAs as acting only as oncogenes in this type of cancer by inhibiting apoptosis and promoting cell cycle and drug resistance. Additionally, here, we discuss how these molecules could be detected in the plasma of T-ALL patients, highlighting that lncRNAs may represent a new class of promising accurate and sensitive biomarkers in these young patients. Thus, the unveiling of the aberrant signature of circulating and intracellular levels of lncRNAs could have great clinical utility for obtaining a more accurate definition of prognosis and uncovering novel therapeutic strategies against T-ALL in children. However, further investigations are needed to better define the standard methodological procedure for their quantification and to obtain their specific targeting in T-ALL pediatric patients.

Breast cancer (BC) remains one of the most prevalent malignancies and leading causes of cancer-related deaths among women worldwide. MicroRNA-204-5p (miR-204-5p) has been implicated in various cancers, where its downregulation is associated with adverse clinicopathological features and poor prognosis. Ezrin, a member of the ERM (Ezrin-Radixin-Moesin) family, links membrane proteins to the actin cytoskeleton and has been reported to play roles in tumor progression. However, the regulatory relationship between miR-204-5p and Ezrin in breast cancer remains unclear.

We conducted bioinformatics analyses using the TCGA BRCA dataset and GEO datasets GSE97811 and GSE144534 to evaluate the expression patterns of miR-204-5p and Ezrin. In vitro assays, including cell proliferation, migration, and invasion analyses, were performed to assess the functional effects of miR-204-5p in BC cells. Western blotting and luciferase reporter assays were used to confirm the regulatory relationship between miR-204-5p, Ezrin, and the AKT signaling pathway.

miR-204-5p was significantly downregulated in breast cancer tissues and was associated with aggressive tumor characteristics and poor patient prognosis. Conversely, Ezrin was upregulated in BC tissues and identified as a direct target of miR-204-5p. Overexpression of miR-204-5p inhibited BC cell proliferation, migration, and invasion, while also reducing Ezrin expression. Mechanistic studies indicated that suppression of Ezrin by miR-204-5p led to downregulation of the AKT signaling pathway.

Our findings demonstrate that miR-204-5p functions as a tumor suppressor in breast cancer by targeting Ezrin and inhibiting the AKT pathway. This suggests a potential therapeutic role for miR-204-5p in the treatment of breast cancer.

Non-coding RNAs (ncRNAs) have a significant role in gene regulation, especially in cancer and inflammatory diseases. ncRNAs, such as microRNA, long non-coding RNAs, and circular RNAs, alter the transcriptional, post-transcriptional, and epigenetic gene expression levels. These molecules act as biomarkers and possible therapeutic targets because aberrant ncRNA expression has been directly connected to tumor progression, metastasis, and response to therapy in cancer research. ncRNAs' interactions with multiple cellular pathways, including MAPK, Wnt, and PI3K/AKT/mTOR, impact cellular processes like proliferation, apoptosis, and immune responses. The potential of RNA-based therapeutics, such as anti-microRNA and microRNA mimics, to restore normal gene expression is being actively studied. Additionally, the tissue-specific expression patterns of ncRNAs offer unique opportunities for targeted therapy. Specificity, stability, and immune responses are obstacles to the therapeutic use of ncRNAs; however, novel strategies, such as modified oligonucleotides and targeted delivery systems, are being developed. ncRNA profiling may result in more individualized and successful treatments as precision medicine advances, improving patient outcomes and creating early diagnosis and monitoring opportunities. The current review aims to investigate the roles of ncRNAs as potential biomarkers and therapeutic targets in cancer and inflammatory diseases, focusing on their mechanisms in gene regulation and their implications for non-invasive diagnostics and targeted therapies. A comprehensive literature review was conducted using PubMed and Google Scholar, focusing on research published between 2014 and 2025. Studies were selected based on rigorous inclusion criteria, including peer-reviewed status and relevance to ncRNA roles in cancer and inflammatory diseases. Non-English, non-peer-reviewed, and inconclusive studies were excluded. This approach ensures that the findings presented are based on high-quality and relevant sources.

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death worldwide. Although many therapeutic modalities have been established for treating HCC patients, the outcomes of patients remain unsatisfactory. Development of independent prognostic biomarkers is thus an important need to allow for early diagnosis and timely treatment. MicroRNAs (miRNAs) are the most studied class of small non-coding RNAs. It has been shown that miRNAs play essential roles in the multiple steps of HCC tumorigenesis and progression. Furthermore, the baseline expression levels of many miRNAs are altered in tumor tissues and blood circulation of HCC patients. Therefore, miRNAs have emerged as independent biomarkers for the prediction of HCC prognosis. This review provides a comprehensive literature-based summary of tissue and circulating miRNA biomarkers with independent prognostic significance in HCC.

A Bhas42 cell transformation assay is a method used to detect the tumour-promoting activities of chemicals. However, the mechanisms underlying tumour transformations mediated by non-genotoxic carcinogens (NGCs) are poorly understood. This study aimed to examine the correlation between 12-O-tetradecanoylphorbol 13-acetate (TPA) or mezerein and the initiation of tumourous transformations by epigenetic regulation in Bhas42 cells. We found that TPA and mezerein prompted tumourous transformations by stimulating cell proliferation and migration in Bhas42 cells. Furthermore, we observed alterations in the expression levels of 134 genes, with 87 genes being upregulated and 47 genes being downregulated, following exposure to either TPA or mezerein. Among the differentially regulated genes, we identified 17 upregulated genes and 8 downregulated genes corresponding to differentially expressed genes in TNM [primary tumour (T), regional nodes (N), and metastasis (M)]. Importantly, we found that TPA and mezerein triggered the expression of Hmga2 and Ezh2 by loss of miRNA let-7 (miR let-7) in Bhas42 cells. Finally, the microRNA (miRNA) mimic of let-7 prevented the TPA- and mezerein-induced activation of Hmga2 and Ezh2 in Bhas42 cells. Our findings reveal a connection between tumourous transformations and the epigenetic regulator miR let-7 in NGCs, such as TPA and mezerein in Bhas42 cells. This highlights miR let-7 as a promising therapeutic target for mitigating tumourous transformations induced by NGCs.

The anomalous expression of microRNA poses a serious threat to human life and health safety, and serves as an important biomarker for cancer detection. In this study, a novel magnetic-assisted DNA logic gate nanomachine triggered by miRNA-21 and miRNA-155 was designed based on the trans-cleavage activity of CRISPR/Cas12a activated by a split DNA activator, using only a single crRNA and signal probe, which simplified the detection procedure and complex nucleic acid amplification. The presence of target molecules, miRNA-21 and miRNA-155, can stimulate the DNA walker machine assembled on magnetic beads, which releases activator under the action of DNAzyme. Then the trans-cleavage activity of CRISPR/Cas12a is initiated and the system signal significantly increases. Based on this, an AND logic gate nanomachine was constructed for simultaneous analysis of miRNA-21 and miRNA-155. The detection limits of miRNA-21 and miRNA-15 were 9.00 pM and 42.00 pM, respectively, and this method was successfully applied to miRNA analysis in cell samples. This nanomachine combined the DNA walker with DNA logic circuit and CRISPR/Cas12a system, providing a new approach for simultaneous detection of multiple targets and further expanding the application of gene editing in the analysis and sensing of multiple target substances.

Coregulation of microRNAs (miRNAs) and cancer stem cells (CSCs) is very important in carcinogenesis. miR-127-5p is known to be downregulated in breast cancer. In this study, we aimed to investigate how boric acid (BA), known for its previously unstudied anti-cancer properties, would affect the expression of miR127-5p and genes responsible for breast cancer stem cells (BC-SCs) metastasis. BC-SCs were isolated from human breast cancer cells (MCF-7) by immunomagnetic cell separation and characterized with flow cytometry and sphere formation. The viability of BC-SCs and the determination of its IC50 value in response to boric acid (BA) were assessed via the MTT assay. Boric acid exhibited dose- and time-dependent inhibition of cell viability in cells. The IC50 doses of boric acid in MCF-7 cells and BC-SCs were 45.69 mM and 41.27 mM, respectively. The impact of BA on the expression of metastatic genes and miR127-5p was elucidated through RT-qPCR analysis. While the expression of the COL1A1 (p < 0.05) and VIM (p < 0.01) was downregulated, the expression of the miR-127-5p, ZEB1 (p < 0.01), CDH1 (p < 0.05), ITGB1 (p < 0.05), ITGA5 (p < 0.05), LAMA5 (p < 0.01), and SNAIL (p < 0.05), was up-regulated in dose-treated BC-SCs (p < 0.001) to the RT-qPCR results. Our findings suggest that boric acid could induce miR-127-5p expression. However, it cannot be said that it improves the metastasis properties of breast cancer stem cells.

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related deaths globally, with poor prognosis due to late diagnosis and limited treatment options. In this study, we evaluated the expression of ectonucleoside triphosphate diphosphohydrolase 8 (ENTPD8) in HCC tissues and its clinical significance. Immunohistochemistry, The Cancer Genome Atlas (TCGA) data, and single-cell expression analysis revealed reduced ENTPD8 levels in liver cancer compared to adjacent tissues, with ENTPD8 primarily expressed in tumor cells within the tumor tissue. In vitro assays demonstrated that ENTPD8 inhibits HCC cell proliferation, invasion, and migration. Mechanistically, ENTPD8 regulates programmed death-ligand 1 (PD-L1) expression through miR-214-5p modulation. In vivo, ENTPD8 overexpression combined with anti-PD-L1 treatment enhanced therapeutic efficacy in HCC mouse models. These findings suggest that ENTPD8 may serve as a prognostic marker and therapeutic target for HCC, offering potential strategies for improving treatment outcomes.

Colorectal cancer (CRC) ranks as the second leading cause of cancer-related death globally, impacting both genders equally. The increasing global mortality rates from CRC are strongly linked to contemporary dietary habits, characterized by excessive meat consumption, alcohol intake, and insufficient physical activity. Thus, there is an unprecedented need to develop less hazardous and new therapies for CRC. CRC affects a substantial global population. The main treatments for CRC include chemotherapy and surgical intervention. Nonetheless, the advancement of innovative, safer, and more effective pharmaceuticals for CRC therapy is of paramount importance due to the widespread adverse effects and the dynamic nature of drug resistance. A growing amount of research suggests that natural chemicals may effectively battle CRC and, in certain cases, serve as alternatives to chemotherapeutics. Evidence suggests that miRNAs control important cancer features, including the maintenance of proliferative signals. These features also involve evasion of growth inhibition, resistance to cell death, and immortalization of replication. Additionally, miRNAs play a role in angiogenesis, invasion, and metastasis. Numerous compounds, including those exhibiting cytotoxic and apoptogenic properties against different malignancies, such as CRC, are sourced from diverse marine and medicinal plants. These chemicals stimulate several signaling pathways originating from different phytochemical families. This article evaluates the existing understanding of the anti-CRC capabilities of several phytochemical substances. Furthermore, their impact on several signaling pathways associated with cancer is examined. This article also highlights the potential of medicinal plants as a source of promising anti-CRC chemicals through modulating miRNA expression and the role of nanoparticle-based miRNA therapeutics in enhancing CRC treatment by improving tumor targeting and minimizing off-target effects.

Colorectal cancer liver metastases (CRLM) are the primary cause of mortality in colorectal cancer (CRC) patients, highlighting the importance of understanding the underlying mechanisms. The tumor microenvironment (TME) and its interaction with tumor cells play a crucial role in CRLM progression. Notably, the stability and peak levels of tumor-derived exosomal miRNAs facilitate intercellular communication in the TME. Hepatic stellate cells (HSCs), key liver mesenchymal cells, constitute about 33% of the liver's nonsolid cell population and exhibit plasticity. However, the specific role of tumor-derived exosomal miRNAs in the crosstalk between HSCs and tumor cells during the CRLM process remains unclear. We studied CRC-secreted exosomal miR-1246 and its impact on HSCs, as well as its effects on CRC cell proliferation and metastasis. Our findings demonstrate that CRC-secreted exosomal miR-1246 can be internalized by HSCs, leading to their activation and facilitating the metastatic potential of CRC cells. Mechanistically, exosomal miR-1246 targets INSIG1, resulting in SREBP2 nucleation and cholesterol metabolism alterations. This accumulation of free cholesterol (FC) regulates the TLR4/NF-κB/TGF-β pathway, promoting HSC activation. Activated HSCs, in turn, enhance liver metastasis of CRC cells through the TNFSF13/TNFRSF13B axis. Our study reveals the role of CRC-secreted exosomal miR-1246 in triggering HSC activation and reprogramming the TME, ultimately facilitating liver metastasis in CRC patients. Exosomal miR-1246 could serve as a potential non-invasive biomarker for predicting colorectal cancer liver metastasis, enhancing our understanding of CRC-associated liver metastases.

Single-molecule detection of nucleic acids in body fluids is vital but challenging. This work presents an optical microfiber biosensor with a metal-semiconductor-2D material hybrid nanointerface for single-molecule amplification-free detection of nucleic acids in complex body fluids. By optimizing the nanointerface components, we achieved significant enhancement of the evanescent field, enabling ultrahigh sensitivity at the microfiber surface. It allowed for the detection of DNA molecules at the single-molecule level and could identify single-base-pair mismatches. Utilizing a microscale diameter and millimeter-length design, the biosensor overcomes the limitations associated with nanosensors, providing a practical solution for point-of-care diagnostics. The sensor demonstrated its potential through ultrasensitive detection of HIV nucleic acids in body fluids such as serum, sweat, and saliva. This advancement marks a critical step forward in nucleic acid detection, facilitating early disease diagnosis, personalized medicine, and fundamental biological research, despite challenges posed by the nanosize, chain-like morphology, and environmental interference of nucleic acids.

Colonic neuroendocrine carcinomas (NECs) are highly malignant and invasive with poor prognosis. Long noncoding RNAs (LncRNAs) participate in the tumorigenesis and metastasis of multiple cancers.

To detect the roles and mechanisms of lncRNA prostate cancer associated transcript 6 (PCAT6) in the progression of colonic NEC.

Human NEC and adjacent normal samples were collected for immunohistochemistry staining of CgA and real-time quantitative polymerase chain reaction (RT-qPCR) of PCAT6 mRNA level. Subcutaneous xenograft tumor model and lung metastasis model were established in nude mice. The lung tissues were stained by hematoxylin and eosin to assess pulmonary metastasis. The expression of epithelial-mesenchymal transition (EMT)-related markers and pathway-related genes was measured by RT-qPCR and western blotting. CD56 expression was assessed by immunofluorescence staining. The biological functions of PCAT6 were examined by cell counting kit-8, colony formation assays, Transwell assays and wound healing assays. The interaction between PCAT6 and its potential downstream target was verified by luciferase reporter assays.

LncRNA PCAT6 was upregulated in human NEC samples and LCC-18 cells, and its high expression was positively correlated with poor prognosis in patients with colonic NEC. Additionally, the expression of PCAT6 was positively associated with the proliferation, migration, invasion, and EMT of LCC-18 cells. Moreover, PCAT6 facilitated tumor growth, lung metastasis and EMT in xenografts. Mechanistically, PCAT6 promoted the activation of MAPK to enhance the EMT in colonic NEC by targeting miR-326.

In conclusion, lncRNA PCAT6 accelerates the process of colonic NEC by activating ERK/p38 MAPK signaling through targeting miR-326. These results might provide useful information for exploring the potential therapeutic targets in colonic NEC.

The action and the latent mechanism of HNF1A-AS1 in oral squamous cell carcinoma (OSCC) development were probed. Levels of HNF1A-AS1, microRNA-138 (miR-138) and Cyclin-dependent kinase 6 (CDK6) were examined. In vitro assays were conducted using SCC-4 and SCC15 cells derived from a human SCC of the tongue of a 55-year-old male. In vivo assay was performed by establishing OSCC mouse models. An elevated HNF1A-AS1 was detected in OSCC, and down-expressed HNF1A-AS1 inhibited migration and invasion, and promoted apoptosis in OSCC cells in vitro. HNF1A-AS1 targeted miR-138 to positively regulate the expression of CDK6, a target of miR-138. Knockdown of miR-138 attenuated the action of HNF1A-AS1 silencing on OSCC cell malignant phenotypes. Besides that, overexpression of CDK6 weakened miR-138-mediated anti-cancer functions. Moreover, HNF1A-AS1 knockdown restrained OSCC growth in nude mice. HNF1A-AS1 promoted OSCC tumorigenesis via miR-138/CDK6 pathway, indicating the potential molecular contribution of HNF1A-AS1 on OSCC pathogenesis.

Colorectal cancer (CRC) was the third most common cause of mortality associated with cancer globally. miR-124-3p has been widely acknowledged for its pivotal role as a tumor suppressor in various malignancies. In this study, we aimed to investigate the specific functions and underlying mechanisms of miR-124-3p in CRC cell proliferation, migration and invasion. A comprehensive set of assays, including CCK-8, colony formation, wound healing assays, flow cytometry, RT-qPCR and Western blotting, were conducted to assess the impact of miR-124-3p expression on CRC cell growth. Our investigations into miR-124-3p and its potential target gene ITGB1 were facilitated through bioinformatics analysis and dual-luciferase reporter assays. To further solidify our findings, rescue experiments were executed to validate the role of miR-124-3p in regulating the proliferation, migration, and apoptosis of CRC cells, genes involving Wnt/β-catenin signaling pathway were also detected. Our study revealed that the overexpression of miR-124-3p significantly suppressed both the proliferation and migratory capabilities of CRC cells, while its downregulation had the opposite effect. Notably, ITGB1 was identified as a putative target gene of miR-124-3p, exhibiting an inverse correlation with the expression levels of miR-124-3p. Moreover, the overexpression of ITGB1 was able to abrogate the inhibitory effects exerted by miR-124-3p overexpression on CRC cell proliferation, migration, and Wnt1/β-catenin protein levels. Our results reveal that miR-124-3p targets ITGB1 to regulate CRC cell proliferation and migration may be associated with the Wnt/β-catenin signaling pathway. These findings provide that a miR-124-3p/ITGB1 axis may be a potential target for the treatment of CRC.

Colorectal cancer (CRC) is a serious public health concern worldwide. Immune checkpoint inhibition medication is likely to remain a crucial part of CRC clinical management. This study aims to create new super paramagnetic iron oxide nano-carrier (SPION) that can effectively transport miRNA to specific CRC cell lines. In addition, evaluate the efficiency of this nano-formulation as a therapeutic candidate for CRC. Bioinformatics tools were used to select a promising tumor suppressor miRNA (mir-497-5p). Green route, using Fusarium oxyporium fungal species, manipulated for the synthesis of SPION@Ag@Cs nanocomposite as a carrier of miR-497-5p. That specifically targets the suppression of PD1/PDL1 and CTLA4pathways for colorectal therapy. UV/visible and FTIR spectroscopy, Zeta potential and MTT were used to confirm the allocation of the miR-497 on SPION@Ag@Cs and its cytotoxicity against CRC cell lines. Immunofluorescence was employed to confirm transfection of cells with miR-497@NPs, and the down- regulation of CTLA4 in HT29, and Caco2 cell lines. On the other hand, PDL1 showed a significant increase in colorectal cell lines (HT-29 and Caco-2) in response to mir497-5p@Nano treatment. The data suggest that the mir-497 -loaded SPION@Ag@Cs nano-formulation could be a good candidate for the suppression of CTLA4in CRC human cell lines. Consequently, the targeting miR-497/CTLA4 axis is a potential immunotherapy treatment strategy for CRC.

Esophageal cancer (ESCA) is a common tumor noted in the digestive tract, which is highly malignant due to unclear early symptoms and poor last‑stage treatment effects; its mortality rate is relatively high. MicroRNA (miR) and signal transducer and activator of transcription 3 (STAT3) are key components of cellular signaling pathways; their interaction forms a complex and intricate information network that controls several types of biological behaviors in the cells. In the tumor cell, these signal transduction pathways are abnormally active, indicating that the STAT3 signaling pathway mediated by miRs is involved in the progression of various cancer types. The present review introduces the biological characteristics of miR and STAT3 and their relationship with ESCA. It summarizes the regulation of ESCA by the miR and STAT3 signaling pathways and analyzes the effects of these pathways on proliferation, apoptosis, invasion, metastasis and immune escape of cancer cells, as well as the impact on patient survival and prognosis. The purpose of the present review is to assess the miR/STAT3 signaling pathway in ESCA, improve the understanding of the pathogenesis of ESCA and facilitate the identification of therapeutic targets for ESCA.

T-cell lymphomas represent non-Hodgkin lymphomas distinguished by the uncontrolled proliferation of malignant T lymphocytes. Classifying these neoplasms and the ongoing investigation of their underlying biological mechanisms remains challenging. Significant subtypes encompass peripheral T-cell lymphomas, anaplastic large-cell lymphomas, cutaneous T-cell lymphomas, and adult T-cell leukemia/lymphoma. A systematic literature survey used electronic databases, including PubMed, Springer Link, Google Scholar, and Web of Science. Search keywords included "T-cell lymphoma," "therapeutic approaches," "RNA therapeutics," "microRNA," and "signaling pathways". T-cell lymphomas are believed to arise from a complex interplay of genetic predispositions and environmental factors. Epstein-Barr virus (EBV) and Human T-cell leukemia virus-1 (HTLV-1), have been implicated as potential etiologic agents. While the exact molecular mechanisms are under investigation, T-cell lymphomas are distinguished by aberrant proliferation of T-cells resulting from dysregulated gene expression. Contemporary research has emphasized the significance of non-coding RNAs, including microRNAs and long non-coding RNAs, in the etiology and advancement of T-cell lymphomas. Certain miRNAs function as tumor suppressors (e.g., miR-451, miR-31, miR-150, miR-29a), while others can act as oncogenes (e.g., miR-223, miR-17-92, miR-155). Additionally, lcRNAs are responsible for modulating gene expression, and their influence on T-cell function suggests their potential outcome as therapeutic targets. Current therapeutic strategies for T-cell lymphomas predominantly rely on chemotherapy, with emerging modalities encompassing immunotherapy and targeted therapies. Despite these advancements, a substantial subset of T-cell lymphomas remains challenging to manage, especially those in advanced stages or refractory to conventional treatments. RNA-based therapeutics represent a promising strategy, offering many advantages such as targeted therapy, potential for personalized medicine, reduced side effects, rapid development, and synergy with other therapies while facing challenges in delivery, immune response, and specificity. Future research should focus on improving delivery systems, modulating immune responses, and optimizing production to unlock its full potential. This review comprehensively explored T-cell lymphomas, delving into their classification, pathogenesis, and existing therapeutic options. Additionally, we explore the evolving function of non-coding RNAs in the pathogenesis of T-cell lymphoma. Furthermore, we discuss the potential of RNA-based therapeutics as a promising treatment strategy.

Considering the high degree of malignancy, recurrence rate and poor prognosis, exploring promising targets is an imperious strategy for colorectal carcinoma therapy. Recent studies have indicated that GABPα plays a role in cancer aggressiveness, but its exact function and regulatory mechanisms in colorectal cancer progression remain unclear. This study aims to explore the biological role of GABPα and its upstream regulator, miR-378a-5p, in modulating cancer progression. The expression levels of GABPα and miR-378a-5p were analyzed through comprehensive data mining and qPCR assays. The functional effects of GABPα were assessed using CCK-8, wound healing, transwell invasion assay, tube formation and xenograft model in nude mice. A co-transfection assay was also performed to investigate the regulatory relationship between miR-378a-5p and GABPα. We found that GABPα expression was significantly downregulated in human colorectal cancer tissues and cell lines. Functional assays revealed that GABPα overexpression suppressed the proliferation, migration, invasion and angiogenesis of colorectal cancer cells, and in vivo experiments further confirmed the inhibitory role of GABPα. Additionally, miR-378a-5p was upregulated in colorectal cancer, and GABPα was identified as a direct target of miR-378a-5p, as confirmed by luciferase reporter assays. Furthermore, overexpression of GABPα partially counteracted the enhanced malignant behaviors of cancer cells induced by miR-378a-5p. Our findings suggest that miR-378a-5p promotes the aggressive progression of colorectal cancer by directly targeting GABPα, highlighting this regulatory axis as a potential therapeutic target for colorectal carcinoma.

Sepsis is a syndrome of the systemic inflammatory response caused by infection that can endanger a patient's life. The aim of this study was to explore the molecular mechanism by which bone marrow mesenchymal stem cells-derived exosomes (BMSCs-exo) carrying miR-20a-5p regulate the progression of sepsis.

Clinical samples from sepsis patients were collected. Mouse and cell models of sepsis were induced by lipopolysaccharide (LPS). The levels of related genes and proteins were determined by RT‒qPCR, Western blotting and ELISA. CCK-8 and flow cytometry assays were used to assess cell viability, apoptosis, and markers of macrophage polarization.

In septic patients, miR-20a-5p levels were significantly lower and CXCL12 expression was significantly increased. After LPS induction, M2 polarization of macrophages was significantly reduced, the level of inflammatory factors was increased, and apoptosis was increased. The addition of BMSCs-exo increased the miR-20a-5p level and decreased the expression of CXCL12 in macrophages, thereby promoting macrophage M2 polarization and reducing the levels of inflammatory factors.

This study demonstrated for the first time that BMSCs-exo promoted the polarization of M2 macrophages through the miR-20a-5p/CXCL12 axis, thus alleviating the development of sepsis. These findings provide a new theoretical basis for the targeted treatment of sepsis with exosomes or miR-20a-5p.

Extracellular vesicles (EVs) have emerged as critical mediators of intercellular communication in cancer. These membranous structures, secreted by normal and cancerous cells, carry a cargo of bioactive molecules including microRNAs (miRNAs) that modulate various cellular processes. miRNAs are small non-coding RNAs that play pivotal roles in post-transcriptional gene regulation and have been implicated in cancer initiation, progression, and metastasis. In cancer, tumor-derived EVs transport specific miRNAs to recipient cells, modulating tumorigenesis, growth, angiogenesis, and metastasis. Dysregulation of miRNA expression profiles within EVs contributes to the acquisition of cancer hallmarks that include increased proliferation, survival, and migration. EV miRNAs influence the tumor microenvironment, promoting immune evasion, remodeling the extracellular matrix, and establishing pre-metastatic niches. Understanding the complex interplay between EVs, miRNAs, and cancer holds significant promise for developing novel diagnostic and therapeutic strategies. This chapter provides insights into the role of EV-mediated miRNA signaling in cancer pathogenesis, highlighting its potential as a biomarker for cancer detection, prognosis, and treatment response assessment.

Mitochondrial dysfunctions are closely associated with different types of disease, including cancer. Carnitine acetyltransferase (CRAT) is a mitochondrial-localized enzyme catalyzing the reversible transfer of acyl groups from an acyl-CoA thioester to carnitine and regulates the ratio of acyl-CoA/CoA. Our bioinformatics analysis using public database revealed a significant decrease of CRAT expression in ovarian cancer (OC). However, the functions of CRAT have rarely been investigated in human cancers, especially in OC. Here, we found a frequent down-regulation of CRAT in OC, which is mainly caused by up-regulation of miR-132-5p. Downregulation of CRAT was significantly associated with shorter survival time for patients with OC. Forced expression of CRAT suppressed OC growth and metastasis by inducing cell cycle arrest and epithelial to mesenchymal transition (EMT). By contrast, CRAT knockdown promoted OC growth and metastasis. Mechanistically, we found that CRAT downregulation promoted OC growth and metastasis by increasing mitochondrial biogenesis to facilitate mitochondrial metabolism through reducing the acetylation of peroxisome proliferator-activated receptor-γ coactivator (PGC-1α). In summary, CRAT functions as a critical tumor suppressor in OC progression by enhancing PGC-1α-mediated mitochondrial biogenesis and metabolism, suggesting CRAT as a potential therapeutic target in treatment of OC.

The accuracy and reliability of identified biomarkers in differentiating early non-small cell lung cancer (NSCLC) remain suboptimal, thereby impeding the timely detection of NSCLC.The objective of this research is to examine the expression level and diagnostic utility of miR-668-3p in individuals with NSCLC, along with its effectiveness and predictive capacity in the combined diagnosis of early-stage NSCLC using serum markers.

The research included 117 NSCLC patients and 101 pulmonary nodule patients (controls). Quantitative PCR was employed to assess the expression levels of miR-668-3p in NSCLC patients. The association between miR-668-3p and clinical characteristics and serum biomarker (AFP, CEA, NSE, and CYFRA21-1) levels in NSCLC patients was examined using chi-square tests and Pearson correlation analyses. The ROC curve analysis was conducted to determine the individual and combined diagnostic efficacy of miR-668-3p and serum biomarkers. Additionally, a logistic regression model was utilized to identify risk factors for lung cancer in patients with pulmonary tuberculosis.

The expression level of miR-668-3p was down-regulated in early-stage NSCLC patients compared with the control group, and showed a significant association with serum biomarkers related with disease progression, tumor staging, and lymph node metastasis. The combined detection of miR-668-3p and serum markers demonstrated robust diagnostic efficacy for early NSCLC and effective predictive capabilities for lung cancer occurrence in individuals with pulmonary nodules.

The miR-668-3p has the potential to be a promising biomarker for NSCLC and enhance the accuracy of early NSCLC clinical detection.

Cervical cancer (CC) is a prevalent gynecological malignancy, contributing to a substantial number of fatalities among women. MicroRNAs (miRNAs) have emerged as promising biomarkers with significant potential for the early detection and prognosis of CC.

This study aimed to explore the clinical significance and biological role of miR-615-5p in CC, with the goal of identifying novel biomarkers for this disease.

The levels of miR-615-5p and TMIGD2 mRNA in tissue samples and cells were quantified through quantitative reverse transcription real-time PCR, followed by statistical analyses to investigate the correlation between miR-615-5p and clinical data. The effects of miR-615-5p on the proliferation and metastasis of CC cells were evaluated using the Cell Counting Kit-8 and Transwell assays. The potential mechanism of miR-615-5p was elucidated by bioinformatics analyses and Dual-luciferase reporter assay. Western blotting was employed to measure the protein levels of TMIGD2.

In CC, the downregulation of miR-615-5p was related to poor prognosis and emerged as an independent prognostic factor. The levels of miR-615-5p were reduced in CC cells. miR-615-5p overexpression restrained the proliferation and metastasis of CC cells. Furthermore, TMIGD2 was identified as a target gene regulated by miR-615-5p, and its expression was notably elevated in CC. The influence of miR-615-5p on the biological behaviors of CC cells was mediated through the modulation of TMIGD2.

Downregulation of miR-615-5p was a prognostic indicator of poor prognosis in CC. miR-615-5p exerted its tumor-suppressive effects by inhibiting cell growth and metastasis through the regulation of TMIGD2.

Cancer is a complex genetic disorder characterized by abnormalities in both coding and regulatory non-coding RNAs. microRNAs (miRNAs) are key regulatory non-coding RNAs that modulate cancer development, functioning as both tumor suppressors and oncogenes. miRNAs play critical roles in cancer progression, influencing key processes such as initiation, promotion, and metastasis. They exert their effects by targeting tumor suppressor genes, thereby facilitating cancer progression, while also inhibiting oncogenes to prevent further disease advancement. The miR-10 family, particularly miR-10a-5p and miR-10b-5p (miR-10a/b-5p), is notably involved in cancer progression. Intriguingly, their functions can differ across different cancers, sometimes promoting and at other times suppressing tumor growth depending on the cancer type and target genes. This review explores the dual roles of miR-10a/b-5p as tumor-suppressive miRNAs (TSmiRs) or oncogenic miRNAs (oncomiRs) in various cancers by examining their molecular and cellular mechanisms and their impact on the tumor microenvironment. Furthermore, we discuss the potential of miR-10a/b-5p as therapeutic targets, emphasizing miRNA-based strategies for cancer treatment. The insights discussed in this review aim to advance our understanding of miR-10a/b-5p's roles in tumor biology and their application in developing innovative cancer therapies.

Hepatocellular carcinoma (HCC) is a malignant tumour that poses a serious threat to human health and places a heavy burden on individuals and society. However, the role of GPC1 in the malignant progression of HCC is unknown. In this study, we analysed the expression of GPC1 in HCC, and its association with poor patient prognosis. The effects of GPC1 on the proliferation, invasion and migration of HCC were analysed through cellular functional experiments in vitro and in vivo. Mechanistically, DNA methylation of GPC1 was analysed by DNA extraction, methylation-specific PCR and bisulfite Sanger sequencing (BSP), and the target genes TET1 and miRNA regulating DNA methylation of GPC1 were found through the bioinformatics database. The results revealed that GPC1 was highly expressed in HCC, and its high expression was significantly associated with poor prognosis of HCC patients. Inhibiting the expression of GPC1 can inhibit the proliferation, invasion and migration of HCC cells. GPC1 was hypomethylated in HCC, and its methylation level was regulated by TET1. miR-143-3p can significantly regulated the expression of TET1 and affect the methylation level and protein expression of GPC1. Furthermore, GPC1 also affects the malignant biological behaviour of HCC by regulating the expression of Hippo signalling pathway. In summary, miR-143-3p regulates the expression of TET1, affects the expression of GPC1 through DNA methylation and regulates the malignant progression of HCC via Hippo signalling pathway.