• DCs
• HkEf
• Lactobacillales
• exosomes
• macrophages
• miRNAs

• dendritic cell development
• glucocorticoids
• interferon
• plasmacytoid dendritic cells
• viral infection

• Animals
• Dendritic Cells/immunology
• Dendritic Cells/metabolism
• Mice
• Lymphocytic choriomeningitis virus/immunology
• Lymphocytic Choriomeningitis/immunology
• Lymphocytic Choriomeningitis/genetics
• Lymphocytic Choriomeningitis/virology
• Glucocorticoids/pharmacology
• Glucocorticoids/metabolism
• Mice, Inbred C57BL
• Stem Cells/metabolism
• Interferon Type I/metabolism
• Cell Differentiation
• fms-Like Tyrosine Kinase 3/metabolism
• Genomics

• R01 AI113923 NIAID NIH HHS
• AI145314 HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID)
• AI132122 HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID)
• Learning from Viruses How to Restore Type 1 Interferons in Cancer San Diego Center for Precision Immunotherapy
• R01 AI081923 NIAID NIH HHS
• AI081923 HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID)
• AI113923 HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID)
• R01 AI145314 NIAID NIH HHS
• P01 AI132122 NIAID NIH HHS

• innate immunity
• innate immunity cells
• microRNA‑29
• virus

• MicroRNAs/genetics
• MicroRNAs/immunology
• Humans
• Immunity, Innate/genetics
• Animals
• Signal Transduction
• Virus Diseases/immunology
• Virus Diseases/genetics

• anticancer immunity
• autoimmunity
• biomarkers
• epigenetics
• immunomodulation
• microRNA
• personalized treatment
• transplantation immunology

• Humans
• MicroRNAs/metabolism
• Autoimmune Diseases/genetics
• Autoimmune Diseases/therapy
• Cell Differentiation

• N6-methyladenosine (m6A)
• RNA methylation
• skin cancers
• skin diseases

• immune response
• infection
• intestinal mucosa
• neoplasm
• plasmacytoid dendritic cells
• type I interferons

• Humans
• Dendritic Cells/immunology
• Animals
• Immunity, Innate
• Mice
• Gastrointestinal Tract/immunology

• 82174056 National Natural Science Foundation of China
• National Natural Science Foundation of China

The incidence rate of ulcerative colitis (UC) is increasing annually, and glucocorticoid (GC) resistance (GCR) is a common cause of UC-induced remission failure. Our previous studies have shown that the expression of miR-642a-5p is downregulated in UC with GCR, suggesting that miR-642a-5p may be related to the GC response. Therefore, we investigated the mechanism by which miR-642a-5p regulates the GC response in THP-1 cells.

We found that after treatment with miR-642a-5p mimics and DEX, the expression levels of glucocorticoid receptor (GR) in the nucleus and NF-κB p65 and p50 in the cytoplasm were increased (P < 0.05). miR-642a-5p mimics transfected into THP-1 cells could synergize with dexamethasone (DEX) to reduce lipopolysaccharide (LPS)-induced inflammatory factor levels such as TNF-α, IL-1β, IL-6 and IL-12 (P < 0.05). Bioinformatics analysis and luciferase reporter assays confirmed that TLR4 is a target gene of miR-642a-5p. miR-642a-5p mimic pretreatment enhanced the inhibitory effect of DEX on TLR4 induced by LPS and inhibited the expression of TLR4 on the cell surface (P < 0.05). Additionally, miR-642a-5p further prevented the nuclear import of NF-κB P65 and inhibited the phosphorylation of ERK, p38 and JNK.

These results suggest that miR-642a-5p can inhibit the inflammation by suppressing the TLR4 signalling pathway in THP-1 cells. It also highlights the TLR4 signalling pathway as a potential therapeutic target in anti-inflammation.

•

miR-642a-5p can inhibit the TLR4 signalling pathway induced by LPS and increase the glucocorticoid sensitivity in THP-1 cells.

Dendritic cells (DCs) are professional antigen-presenting cells that act as a bridge between innate immunity and adaptive immunity. After activation, DCs differentiate into subtypes with different functions, at which point they upregulate co-stimulatory molecules and produce various cytokines and chemokines. Activated DCs also process antigens for presentation to T cells and regulate the differentiation and function of T cells to modulate the immune state of the body. Non-coding RNAs, RNA transcripts that are unable to encode proteins, not only participate in the pathological mechanisms of autoimmune-related diseases but also regulate the function of immune cells in these diseases. Accumulating evidence suggests that dysregulation of non-coding RNAs contributes to DC differentiation, functions, and so on, consequently producing effects in various autoimmune diseases. In this review, we summarize the main non-coding RNAs (miRNAs, lncRNAs, circRNAs) that regulate DCs in pathological mechanisms and have tremendous potential to give rise to novel therapeutic targets and strategies for multiple autoimmune diseases and immune tolerance-related diseases.

• autoimmune disease
• ce-RNAs
• dendritic cell
• immune tolerance
• non-coding RNA

• cardiac inflammation3
• heart failure1
• inflammatory cells4
• ncRNAs2

• adeno-associated virus vectors
• antigen presenting cells
• gene therapy
• miR-142
• miR-223-3p
• miR-652-5p
• miR-BS
• microRNA

• Animals
• Antigen Presentation/immunology
• Antigen-Presenting Cells/immunology
• Binding Sites
• Dependovirus
• Female
• Genetic Therapy/methods
• Genetic Vectors
• Male
• Mice
• Mice, Inbred C57BL
• MicroRNAs
• Transduction, Genetic/methods
• Transgenes

• UG3 HL147367 NHLBI NIH HHS
• R01 HL097088 NHLBI NIH HHS
• P01 HL131471 NHLBI NIH HHS
• U19 AI149646 NIAID NIH HHS
• P01 AI100263 NIAID NIH HHS
• R01 AI121135 NIAID NIH HHS
• R01 NS076991 NINDS NIH HHS

Pathogenic mutations in the non-syndromic hearing loss and deafness 1 (DFNB1) locus are the primary cause of monogenic inheritance for prelingual hearing loss. To unravel molecular pathways involved in etiopathology and look for early degeneration biomarkers, we used a system biology approach to analyze Cx30^−/− mice at an early cochlear post-natal developmental stage. These mice are a DFNB1 mouse model with severely reduced expression levels of two connexins in the inner ear, Cx30, and Cx26. Integrated analysis of miRNA and mRNA expression profiles in the cochleae of Cx30^−/− mice at post-natal day 5 revealed the overexpression of five miRNAs (miR-34c, miR-29b, miR-29c, miR-141, and miR-181a) linked to apoptosis, oxidative stress, and cochlear degeneration, which have Sirt1 as a common target of transcriptional and/or post-transcriptional regulation. In young adult Cx30^−/− mice (3 months of age), these alterations culminated with blood barrier disruption in the Stria vascularis (SV), which is known to have the highest aerobic metabolic rate of all cochlear structures and whose microvascular alterations contribute to age-related degeneration and progressive decline of auditory function. Our experimental validation of selected targets links hearing acquisition failure in Cx30^−/− mice, early oxidative stress, and metabolic dysregulation to the activation of the Sirt1–p53 axis. This is the first integrated analysis of miRNA and mRNA in the cochlea of the Cx30^−/− mouse model, providing evidence that connexin downregulation determines a miRNA-mediated response which leads to chronic exhaustion of cochlear antioxidant defense mechanisms and consequent SV dysfunction. Our analyses support the notion that connexin dysfunction intervenes early on during development, causing vascular damage later on in life. This study identifies also early miRNA-mediated biomarkers of hearing impairment, either inherited or age related.

• connexins
• early degeneration
• hearing loss
• molecular pathway analysis
• oxidative stress
• post-natal development
• systems biology
• vascular dysfunction

• Apoptosis
• Peripheral blood monocytes (PBMs)
• Rheumatoid arthritis (RA)
• TNF-α
• miRNA

A considerable body of evidence supports a role for type-I IFN in the pathogenesis of primary SS (pSS). As plasmacytoid dendritic cells (pDCs) are a major source of type-I IFN, we investigated their molecular regulation by measuring expression of a large set of miRNAs.

pDCs were isolated from peripheral blood of pSS patients (n = 30) and healthy controls (n = 16) divided into two independent cohorts (discovery and replication). Screening of 758 miRNAs was assessed by an OpenArray quantitative PCR-based technique; replication of a set of identified miRNAs was performed by custom array. Functional annotation of miRNA targets was performed using pathway enrichment. Novel targets of miR-29a and miR-29c were identified using a proteomic approach (stable isotope labelling with amino acids in cell culture).

In the discovery cohort, 20 miRNAs were differentially expressed in pSS pDCs compared with healthy control pDCs. Of these, differential expression of 10 miRNAs was confirmed in the replication cohort. The dysregulated miRNAs were involved in phosphoinositide 3-kinase-Ak strain transforming and mammalian target of rapamycin signalling, as well as regulation of cell death. In addition, a set of novel protein targets of miR-29a and miR-29c were identified, including five targets that were regulated by both miRs.

The dysregulated miRNome in pDCs of patients with pSS is associated with aberrant regulation of processes at the centre of pDC function, including type-I IFN production and cell death. As miR-29a and miR-29c are pro-apoptotic factors and several of the novel targets identified here are regulators of apoptosis, their downregulation in patients with pSS is associated with enhanced pDC survival.

• Sjögren’s syndrome
• microRNAs
• plasmacytoid dendritic cells
• type-I interferon

• Antigen-presenting cells
• DNA methylation
• Histone modification
• Systemic lupus erythematosus
• noncoding RNA

• DNA methylation
• Histone modifications
• Lupus
• lncRNAs
• microRNAs

• digestive signs and symptoms
• ulcerative colitis
• experimental models of disease

• Animals
• Colitis/chemically induced
• Colitis/diet therapy
• Colitis/immunology
• Colitis/pathology
• Dextran Sulfate/toxicity
• Dietary Supplements
• Disease Models, Animal
• Extracellular Vesicles/immunology
• Gastrointestinal Microbiome/immunology
• Humans
• Intestinal Mucosa/immunology
• Intestinal Mucosa/microbiology
• Intestinal Mucosa/pathology
• Male
• Mice
• Milk/cytology
• Milk/immunology
• Mucins/metabolism
• Ultracentrifugation

• 319618 Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de Recherche en Santé du Canada)
• 327522 Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de Recherche en Santé du Canada)
• 421606 Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de Recherche en Santé du Canada)
• IG1-134171 CIHR
• MOP-137081 CIHR
• PJT-165806 CIHR
• 156205 CIHR
• Fonds de Recherche du Québec - Santé (Fonds de la recherche en sante du Quebec)

Mesenchymal stromal cells (MSCs) are potent regulators of immune responses largely through paracrine signaling. MSC secreted extracellular vesicles (MSC-EVs) are increasingly recognized as the key paracrine factors responsible for the biological and therapeutic function of MSCs. We report the first comprehensive study demonstrating the immunomodulatory effect of MSC-EVs on dendritic cell (DC) maturation and function. MSC-EVs were isolated from MSC conditioned media using differential ultracentrifugation. Human monocyte-derived DCs were generated in the absence or presence of MSC-EVs (20 ug/ml) then subjected to phenotypic and functional analysis in vitro. MSC-EV treatment impaired antigen uptake by immature DCs and halted DC maturation resulting in reduced expression of the maturation and activation markers CD83, CD38, and CD80, decreased secretion of pro-inflammatory cytokines IL-6 and IL-12p70 and increased production of anti-inflammatory cytokine TGF-β. MSC-EV treated DCs also demonstrated a diminished CCR 7 expression after LPS stimulation, coupled with a significantly reduced ability to migrate toward the CCR7-ligand CCL21, although they were still able to stimulate allogeneic T cell proliferation in vitro. Through microRNA profiling we have identified 49 microRNAs, which were significantly enriched in MSC-EVs compared to their parent MSCs. MicroRNAs with known effect on DC maturation and functions, including miR-21-5p, miR-142-3p, miR-223-3p, and miR-126-3p, were detected within the top 10 most enriched miRNAs in MSC-EVs, with MiR-21-5p as the third highest expressed miRNA in MSC-EVs. In silico analysis revealed that miR-21-5p targets the CCR7 gene for degradation. To verify these observations, DCs were transfected with miR-21-5p mimics and analyzed for their ability to migrate toward the CCR7-ligand CCL21 in vitro. MiR-21-5p mimic transfected DCs showed a clear trend of reduced CCR7 expression and a significantly decreased migratory ability toward the CCL21. Our findings suggest that MSC-EVs are able to recapitulate MSC mediated DC modulation and MSC-EV enclosed microRNAs may represent a novel mechanism through which MSCs modulate DC functions. As MSCs are currently used in clinical trials to treat numerous diseases associated with immune dysregulation, such as graft-versus-host disease and inflammatory bowel disease, our data provide novel evidence to inform potential future application of MSC-EVs as a cell-free therapeutic agent.

• dendritic cells
• extracellular vesicles
• immunomodulation
• mesenchymal stromal cells
• microRNA

• glucocorticoids
• inflammatory bowel disease
• mRNA
• pediatric patients

• Adolescent
• Biomarkers
• Child
• Female
• Gene Expression Regulation/drug effects
• Glucocorticoids/administration & dosage
• Glucocorticoids/adverse effects
• High-Throughput Nucleotide Sequencing
• Humans
• Inflammatory Bowel Diseases/drug therapy
• Inflammatory Bowel Diseases/genetics
• Inflammatory Bowel Diseases/pathology
• Male
• MicroRNAs/genetics
• Receptors, Glucocorticoid/genetics
• Transcriptome/drug effects

• Autoimmune diseases
• Biomarkers
• Epigenetics
• SLE

The proliferation and apoptosis of pulmonary artery smooth muscle cells (PASMCs) are considered to be key steps in the progression of pulmonary arterial hypertension (PAH). MicroRNAs (e.g., miR-29b) have been identified in various diseases to be critical modulators of cell growth and apoptosis by targeting Mcl-1 and CCND2. However, the role of miR-29b in PAH remains unknown. So we try to investigate the effect of miR-29b on Mcl-1 and CCND2 protein in PASMCs, analyze the effect of miR-29b on the proliferation of PASMCs, and explore the significance of miR-29b in the proliferation, apoptosis, and gene therapy of PAH. It was observed that gene chip analysis showed miR-29b expression in pulmonary artery tissue. The expression of miR-29b was significantly reduced in PAH model mice. MiR-29b inhibited the proliferation of PASMCs and promoted the apoptosis of PASMCs. Mechanically, miR-29b could inhibit the expression of Mcl-1 and CCND2 protein and silenced Mcl-1 and CCND2 could abolish the change of proliferation and apoptosis of PASMCs. These results demonstrate that miR-29b suppressed cellular proliferation and promoted apoptosis of PASMCs, possibly through the inhibition of Mcl-1 and CCND2. Therefore, miR-29b may serve as a useful therapeutic tool to treat PAH.

Glucocorticoids (GCs) are steroids with profound anti-inflammatory and immunomodulatory activities. Synthetic GCs are widely used for managing chronic inflammatory and autoimmune conditions, as immunosuppressants in transplantation, and as anti-tumor agents in certain hematological cancers. However, prolonged GC exposure can cause adverse effects. A detailed understanding of GCs' mechanisms of action may enable harnessing of their desirable actions while minimizing harmful effects. Here, we review the impact on the GC biology of microRNAs, small non-coding RNAs that post-transcriptionally regulate gene expression. Emerging evidence indicates that microRNAs modulate GC production by the adrenal glands and the cells' responses to GCs. Furthermore, GCs influence cell proliferation, survival, and function at least in part by regulating microRNA expression. We propose that the beneficial effects of GCs may be enhanced through combination with reagents targeting specific microRNAs.

• apoptosis
• epigenetics
• glucocorticoid
• glucocorticoid receptor
• inflammation
• microRNA (miRNA)

• SLE
• apoptosis
• autophagy
• cell death
• epigenetics
• necrosis

• Apoptosis/genetics
• Apoptosis/immunology
• Autoantibodies/immunology
• Autoantigens/immunology
• Autophagy/genetics
• Autophagy/immunology
• DNA Methylation/genetics
• Dendritic Cells/immunology
• Epigenesis, Genetic/genetics
• Humans
• Lupus Erythematosus, Systemic/genetics
• Lupus Erythematosus, Systemic/immunology
• Lupus Erythematosus, Systemic/pathology
• Macrophages/immunology
• Necrosis/genetics
• Necrosis/immunology

Systemic inflammatory rheumatic diseases are considered as autoimmune diseases, meaning that the balance between recognition of pathogens and avoidance of self-attack is impaired and the immune system attacks and destroys its own healthy tissue. Treatment with conventional Disease Modifying Antirheumatic Drugs (DMARDs) and/or Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) is often associated with various adverse reactions due to unspecific and toxic properties of those drugs. Although biologic drugs have largely improved the outcome in many patients, such drugs still pose significant problems and fail to provide a solution to all patients. Therefore, development of more effective treatments and improvements in early diagnosis of rheumatic diseases are badly needed in order to increase patient's functioning and quality of life. The reversible nature of epigenetic mechanisms offers a new class of drugs that modulate the immune system and inflammation. In fact, epigenetic drugs are already in use in some types of cancer or cardiovascular diseases. Therefore, epigenetic-based therapeutics that control autoimmunity and chronic inflammatory process have broad implications for the pathogenesis, diagnosis, and management of rheumatic diseases. This review summarises the latest information about potential therapeutic application of epigenetic modification in targeting immune abnormalities and inflammation of rheumatic diseases.

• microRNAs
• plasmacytoid dendritic cells
• systemic lupus erythematosus
• toll-like receptor 7

• Animals
• Antigen Presentation
• Bone Marrow Cells/metabolism
• CD40 Antigens/genetics
• CD40 Antigens/metabolism
• Cells, Cultured
• Dendritic Cells/metabolism
• Female
• Gene Expression
• Lupus Erythematosus, Systemic/metabolism
• Membrane Glycoproteins/metabolism
• Mice, Transgenic
• MicroRNAs/physiology
• RNA Interference
• Toll-Like Receptor 7/metabolism

• apoptosis
• diabetes mellitus
• endothelial dysfunction
• hyperglycemia
• microRNA

Dendritic cells (DC) play an important role in the pathogenesis of systemic lupus erythematosus (SLE), an autoimmune disease with multiple tissue manifestations. In this review, we summarize recent studies on the roles of conventional DC and plasmacytoid DC in the development of both murine lupus and human SLE. In the past decade, studies using selective DC depletions have demonstrated critical roles of DC in lupus progression. Comprehensive in vitro and in vivo studies suggest activation of DC by self-antigens in lupus pathogenesis, followed by breakdown of immune tolerance to self. Potential treatment strategies targeting DC have been developed. However, many questions remain regarding the mechanisms by which DC modulate lupus pathogenesis that require further investigations.

Inflammatory bowel disease (IBD) is characterized by chronic relapsing inflammatory disorders of the gastrointestinal tract, and includes two major phenotypes: ulcerative colitis and Crohn’s disease. The pathogenesis of IBD is not fully understood as of yet. It is believed that IBD results from complicated interactions between environmental factors, genetic predisposition, and immune disorders. miRNAs are a class of small non-coding RNAs that can regulate gene expression by targeting the 3′-untranslated region of specific mRNAs for degradation or translational inhibition. miRNAs are considered to play crucial regulatory roles in many biologic processes, such as immune cellular differentiation, proliferation, and apoptosis, and maintenance of immune homeostasis. Recently, aberrant expression of miRNAs was revealed to play an important role in autoimmune diseases, including IBD. In this review, we discuss the current understanding of how miRNAs regulate autoimmunity and inflammation by affecting the differentiation, maturation, and function of various immune cells. In particular, we focus on describing specific miRNA expression profiles in tissues and peripheral blood that may be associated with the pathogenesis of IBD. In addition, we summarize the opportunities for utilizing miRNAs as new biomarkers and as potential therapeutic targets in IBD.

• Autoimmunity
• Immune system
• Inflammation
• Inflammatory bowel disease
• miRNA

• Animals
• Autoimmunity
• Genetic Markers
• Humans
• Immunity, Innate
• Inflammation Mediators/immunology
• Inflammation Mediators/metabolism
• Inflammatory Bowel Diseases/genetics
• Inflammatory Bowel Diseases/immunology
• Inflammatory Bowel Diseases/metabolism
• Inflammatory Bowel Diseases/therapy
• Intestinal Mucosa/metabolism
• Intestines/immunology
• MicroRNAs/genetics
• MicroRNAs/immunology
• MicroRNAs/metabolism
• Signal Transduction

• Animal models
• Autoimmune disease
• Circulating microRNA
• Immune system
• Immunomodulation

• plasmacytoid dendritic cell
• interferon
• transcription factor
• virus
• autoimmunity
• cancer
• mucosal immunity
• human

• Adaptive Immunity
• Animals
• Antigen Presentation
• Autoimmune Diseases/immunology
• Autoimmune Diseases/pathology
• Autoimmunity
• Cytokines/genetics
• Cytokines/immunology
• Dendritic Cells/immunology
• Dendritic Cells/pathology
• Dendritic Cells/virology
• Gene Expression Regulation
• Humans
• Immunity, Innate
• Interferon Type I/genetics
• Interferon Type I/immunology
• Mice
• Signal Transduction
• Virus Diseases/immunology
• Virus Diseases/pathology
• Virus Diseases/virology

• K01 DK095972 NIDDK NIH HHS
• K01DK095972 NIDDK NIH HHS

• WNT signaling
• glucocorticoids
• microRNA-199a-5p
• osteoblasts
• proliferation

• 3T3 Cells
• Animals
• Base Sequence
• Binding Sites
• Cell Differentiation
• Cell Proliferation
• Dexamethasone/pharmacology
• Female
• Frizzled Receptors/genetics
• Frizzled Receptors/metabolism
• Glucocorticoids/pharmacology
• Mice
• Mice, Inbred C57BL
• MicroRNAs/physiology
• Osteoblasts/physiology
• RNA Interference
• Up-Regulation
• Wnt Signaling Pathway
• Wnt2 Protein/genetics
• Wnt2 Protein/metabolism

• DNA methylation
• SLE
• epigenetics
• histone modification
• microRNA

• B-Lymphocytes/immunology
• B-Lymphocytes/metabolism
• DNA Methylation
• Epigenesis, Genetic
• Histone Deacetylase Inhibitors/therapeutic use
• Histones/chemistry
• Histones/metabolism
• Humans
• Lupus Erythematosus, Systemic/drug therapy
• Lupus Erythematosus, Systemic/genetics
• Lupus Erythematosus, Systemic/pathology
• MicroRNAs/metabolism
• T-Lymphocytes/immunology
• T-Lymphocytes/metabolism

• dendritic cells
• immune modulation
• microRNAs

Glucocorticoids (GCs) selectively trigger cell death in the multiple myeloma cell line MM1S which express NR3C1/Glucocorticoid Receptor (GR) protein, but fail to kill MM1R cells which lack GR protein. Given recent demonstrations of altered microRNA profiles in a diverse range of haematological malignancies and drug resistance, we characterized GC inducible mRNA and microRNA transcription profiles in GC sensitive MM1S as compared to GC resistant MM1R cells. Transcriptome analysis revealed that GCs regulate expression of multiple genes involved in cell cycle control, cell organization, cell death and immunological disease in MM1S cells, which remain unaffected in MM1R cells. With respect to microRNAs, mir-150-5p was identified as the most time persistent GC regulated microRNA, out of 5 QPCR validated microRNAs (mir-26b, mir-125a-5p, mir-146-5p, mir-150-5p, and mir-184), which are GC inducible in MM1S but not in MM1R cells. Functional studies further revealed that ectopic transfection of a synthetic mir-150-5p mimics GR dependent gene expression changes involved in cell death and cell proliferation pathways. Remarkably, despite the gene expression changes observed, overexpression of mir-150-5p in absence of GCs did not trigger significant cytotoxicity in MM1S or MM1R cells. This suggests the requirement of additional steps in GC induced cell death, which can not be mimicked by mir-150-5p overexpression alone. Interestingly, a combination of mir-150-5p transfection with low doses GC in MM1S cells was found to sensitize therapy response, whereas opposite effects could be observed with a mir-150-5p specific antagomir. Although mir-150-5p overexpression did not substantially change GR expression levels, it was found that mir-150-5p evokes GR specific effects through indirect mRNA regulation of GR interacting transcription factors and hormone receptors, GR chaperones, as well as various effectors of unfolded protein stress and chemokine signalling. Altogether GC-inducible mir-150-5p adds another level of regulation to GC specific therapeutic responses in multiple myeloma.

• Adult
• Apoptosis/drug effects
• Cell Cycle Checkpoints/drug effects
• Cell Line, Tumor
• Cell Proliferation/drug effects
• Chemokines/metabolism
• DNA Damage/drug effects
• Dexamethasone/pharmacology
• Down-Regulation/drug effects
• Female
• Humans
• MicroRNAs/antagonists & inhibitors
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Multiple Myeloma/metabolism
• Multiple Myeloma/pathology
• Oligonucleotides, Antisense/metabolism
• TOR Serine-Threonine Kinases/metabolism
• Transfection
• Up-Regulation/drug effects

• Gastric cancer
• Genetic susceptibility
• LAMTOR3
• Single nucleotide polymorphism
• miR-29c

• Biomarkers
• DNA methylation
• HDAC inhibitors
• Pharmacoepigenetics
• Systemic lupus erythematosus (SLE)
• microRNA