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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: .
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Does microRNA-26b regulate cancer proliferation migration and cell cycle transition by suppressing TRAF5 in esophageal squamous cell carcinoma? Context: MicroRNAs have been identified to play important role in the development of human esophageal squamous carcinoma (ESCC). In this study, we examined the regulatory effects of microRNA-26b (miR-26b) on ESCC proliferation, cell-cycle transition and migration. Expressions of miR-26a and miR-2bb were analyzed in 8 ESCC cell lines, and 27 human ESCC tissues and paired adjacent non-tumor tissues. MiR-26a and miR-26b were either upregulated or downregulated in ESCC cell lines TE-1 and Kyse140 cells. Their effects on ESCC in vitro growth, cell-cycle transition and migration were analyzed by proliferation assay, cell-cycle assay and invasion assay, respectively. The association of miR-26b and its downstream target gene, tumor necrosis factor receptor-associated factor 5 (TRAF5), was analyzed by luciferase reporter assay and qRT-PCR. TRAF5 was downregulated in TE-1 and Kyse140 cells to analyze its direct effect on miR-26b downregulation induced ESCC inhibition. MiR-26b expression was aberrantly upregulated in ESCC cell lines and human ESCC tissues, whereas miR-26a expression was unchanged. In TE-1 and Kyse140 cells, miR-26b downregulation had tumor-suppressive effect, whereas miR-26b downregulation or miR-26a upregulation/downregulation had no significant effect, on ESCC proliferation, cell-cycle transition and migration. TRAF5 is confirmed to be the downstream target of miR-26b in ESCC. SiRNA-mediated TRAF5 downregulation inversely regulated the inhibition of miR-26b downregulation on ESCC proliferation, cell-cycle transition and migration.
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our study demonstrates that miR-26b downregulation, through the inverse regulation on TRAF5, had tumor-suppressive effect on human ESCC. Final Decision: yes