Zhuo Chen1, Liang Zhao2, Feng Zhao1, Guanghai Yang1, Jianjun Wang1. 1. Department of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology 1277 Jie Fang Avenue, Wuhan 430022, China. 2. Department of Thoracic Surgery, The Central Hospital of Wuhan, Tongji Medical College of Huazhong University of Science and Technology Wuhan 430030, China.
Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: our study demonstrates that miR-26b downregulation, through the inverse regulation on TRAF5, had tumor-suppressive effect on human ESCC.
BACKGROUND: MicroRNAs have been identified to play important role in the development of humanesophageal squamous carcinoma (ESCC). In this study, we examined the regulatory effects of microRNA-26b (miR-26b) on ESCC proliferation, cell-cycle transition and migration. METHODS: 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. RESULTS: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. CONCLUSION: our study demonstrates that miR-26b downregulation, through the inverse regulation on TRAF5, had tumor-suppressive effect on human ESCC.
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