Chloroxylenol is a worldwide commonly used disinfectant. The massive consumption and relatively high chemical stability of chloroxylenol have caused eco-toxicological threats in receiving waters. We noticed that chloroxylenol has a chemical structure similar to numerous halo-phenolic disinfection byproducts. Solar detoxification of some halo-phenolic disinfection byproducts intrigued us to select a rapidly degradable chloroxylenol alternative from them. In investigating antimicrobial activities of disinfection byproducts, we found that 2,6-dichlorobenzoquinone was 9.0-22 times more efficient than chloroxylenol in inactivating the tested bacteria, fungi and viruses. Also, the developmental toxicity of 2,6-dichlorobenzoquinone to marine polychaete embryos decreased rapidly due to its rapid degradation via hydrolysis in receiving seawater, even without sunlight. Our work shows that 2,6-dichlorobenzoquinone is a promising disinfectant that well addresses human biosecurity and environmental sustainability. More importantly, our work may enlighten scientists to exploit the slightly alkaline nature of seawater and develop other industrial products that can degrade rapidly via hydrolysis in seawater.

Colorectal cancer (CRC) remains one of the most commonly diagnosed cancers and a leading cause of cancer-related deaths worldwide. The stepwise accumulation of epigenetic alterations in the normal colorectal epithelium has been reported to act as a driving force for the initiation and promotion of tumorigenesis in CRC. From a mechanistic standpoint, emerging evidence indicates that within the colorectal epithelium, the diverse gut microbiota can interact with host cells to regulate multiple physiological processes. In fact, recent studies have found that the gut microbiota represents a potential cause of carcinogenesis, invasion, and metastasis via DNA methylation, histone modifications, and non-coding RNAs - providing an epigenetic perspective for the connection between the gut microbiota and CRC. Herein, we comprehensively review the recent research that provides a comprehensive yet succinct evidence connecting the gut microbiota to CRC at an epigenetic level, including carcinogenic mechanisms of cancer-related microbiota, and the potential for utilizing the gut microbiota as CRC biomarkers. These scientific findings highlight a promising future for manipulating the gut microbiota to improve clinical outcomes in patients suffering from CRC.

Infections of Salmonella typhimurium (S. typhimurium) are major threats to health, threats include diarrhoea, fever, acute intestinal inflammation, and cancer. Nevertheless, little information is available about the involvement of S. typhimurium in colon cancer etiology.

The present study was designed to predict nuclear targeting of S. typhimurium proteins in the host cell through computational tools, including nuclear localization signal (NLS) mapper, Balanced Subcellular Localization predictor (BaCeILo), and Hum-mPLoc using next-generation sequencing data.

Several gene expression-associated proteins of S. typhimurium have been predicted to target the host nucleus during intracellular infections. Nuclear targeting of S. typhimurium proteins can lead to competitive interactions between the host and pathogen proteins with similar cellular substrates, and it may have a possible involvement in colon cancer growth. Our results suggested that S. typhimurium releases its proteins within compartments of the host cell, where they act as a component of the host cell proteome. Protein targeting is possibly involved in colon cancer etiology during intracellular bacterial infection.

The results of current in-silico study showed the potential involvement of S. typhimurium infection with alteration in normal functioning of host cell which act as possible factor to connect with the growth and development of colon cancer.

Colorectal cancer (CRC) is the third most common cancer in men (746000 cases per year) and the second most common cancer in women globally (614000 cases per year). The incidence rate of CRC in developed countries (737000 cases per year) is higher than that in less developed countries (624000 cases per year). CRC can arise from genetic causes such as chromosomal instability and microsatellite instability. Several etiologic factors underlie CRC including age, diet, and lifestyle. Gut microbiota represent a proven cause of the disease, where they play pivotal roles in modulating and reshaping the host epigenome. Several active microbial metabolites have been found to drive carcinogenesis, invasion, and metastasis via modifying both the methylation landscape along with histone structure in intestinal cells. Gut microbiota, in response to diet, can exert both beneficial and harmful functions in humans, according to the intestinal balance of number and types of these bacteria. Although the intestinal microbial community is diverse among individuals, these microbes cumulatively produce 100-fold more proteins than the human genome itself, which calls for further studies to elaborate on the complicated interaction between these microorganisms and intestinal cells. Therefore, understanding the exact role that gut microbiota play in inducing CRC will help attain reliable strategies to precisely diagnose and treat this fatal disease.