The cell surface membrane-bound mucin protein MUC4 promotes tumorigenicity, aggressive behavior, and poor outcomes in various types of epithelial carcinomas, including pancreatic, breast, colon, ovarian, and prostate cancer. This review summarizes the theories and findings regarding MUC4 function, and its role in epithelial carcinogenesis. Based on these insights, we developed an outline of the processes and mechanisms by which MUC4 critically supports the propagation and survival of cancer cells in various epithelial organs. MUC4 may therefore be a useful prognostic and diagnostic tool that improves our ability to eradicate various forms of cancer.

Adherent-invasive Escherichia coli (AIEC) has recently attracted more attention because it is closely related to the pathogenicity of human inflammatory bowel disease (IBD). AIEC possesses a multitude of virulence factors. Considering these virulence factors belonging to various virulence groups, including adhesins, invasins, toxins, protectins, and siderophore-mediated iron acquisition, this review summarizes the current knowledge of how the major virulence factors assisting in AIEC survive in, adhere to, and invade host cells. A comprehensive understanding of the interaction of virulence factors with host cells will provide us a new therapeutic strategy for IBD prevention and treatment.

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Purpose. -Pancreatic β-cell failure is a central hallmark of the pathogenesis of diabetes mellitus; however, the molecular basis underlying chronic in ammation-caused β-cell failure remains unclear. This study reported here speci cally assessed the association between miR-25/miR-92b family and β-cell failure in diabetes.Methods. -IL-1β and two additional ER stress activators, palmitate and tunicamycin were applied to evaluate the expression level miR-25 by Taqman ® RT-PCR. Glucose-and potassium-stimulated insulin secretion assays were performed to assess β-cell function. Dual luciferase activity, and western blotting assays were utilized for miR-25 target gene veri cation. CCK-8 and TUNEL staining were used to evaluate β-cell viability and apoptosis. Results. -miRNA ChIP identi ed the increased level of miR-25 in INS-1 cells by IL-1β treatment. Expression levels of miR-25 were signi cantly upregulated with the treatment of IL-1β, palmitate or tunicamycin in both INS-1 cells and human islets. Ectopic elevation of miR-25 recapitulated most featured β-cell defects caused by IL-1β, including inhibition of insulin biosynthesis and increased β-cell apoptosis. These detrimental effects of miR-25 relied on its seed sequence recognition and repressed expression of its target genes Neurod1 and Mcl1. The miR-25/NEUROD1 axis reduced insulin biosynthesis via transcriptional regulation of β-cell speci c genes. The miR-25/MCL1 axis caused β-cell apoptosis in a caspase 3/PARP1-dependent manner. Comparable impairments were generated by miR-92b and miR-25, emphasizing the redundant biological roles of miRNA family members with the same seed sequence. Conclusion. -MiR-25/miR-92b family plays a major role in β-cell failure occurring under in ammation and diabetes states.Total RNA was extracted using TRIzol reagent (Invitrogen). Then Affymetrix miRNA ChIP was applied to ltrate abundance assessment of miRNA. TaqMan ® probes (Ambion, Foster City, CA) was used to detect miR-25 expression by using the THUNDERBIRD probe qPCR Mix (TOYOBO). For mRNA expression, SYBR Green qPCR Master Mix was used. The miRNA and mRNA expressions were detected on Roche Lightcycle480 II Sequence Detection System (Roche, Basel, Switzerland). Methods of miRNA and mRNA expression analysis were as described previously [12]. U6 and Actb were used as internal standards for miRNAs and mRNAs, respectively. Primers used are as follows:

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