BACKGROUND: MicroRNAs are emerging as the important regulators in cancer-related processes. This research were performed to find the function and mechanism of miR-34a effect on colon cancer. METHODS: In this study, we examined the expression of miR-34a in colon cancer tissues and cell lines by qRT-PCR. In vitro cell functional assays studies were built to define miR-34a and SYT1 function involved in cell growth, migration, and invasion and apoptosis. EGFP reporter assay was used to determine the relationship of SYT1 and miR-181a. To confirmed the relationship between SYT1 and miR-34a, the SYT1 restoration rescued miR-34a mediated growth and inhibited cell apoptosis were detect. RESULT: Our studies show that microRNA-34a (miR-34a) is downregulated in human colon cancer relative to normal colon mucosal epithelial cells, and downexpression of miR-34a promotes cell proliferation, migration, and invasion, nevertheless overexpression of miR-34 facilitates cell apoptosis in vitro. Furthermore, SYT1 3'-UTR is found to be down-regulated directly by miR-34a, demonstrating that SYT1 is a important target of miR-34a in colon cancer. The knockdown of SYT1 markedly inhibits colon cancer cell proliferation, migration, and invasion, and induces cell apoptosis, indicating that SYT1 may function as an oncogene in colon cancer. The restoration of SYT1 expression can counteract the effect of miR-34a on cell proliferation, and induces cell apoptosis, of colon cancer cells. CONCLUSION: Together, these results indicate that miR-34a is a new regulator of SYT1, and both miR-34a and SYT1 play the important roles in the pathogenesis of colon cancer. IJCEP
BACKGROUND: MicroRNAs are emerging as the important regulators in cancer-related processes. This research were performed to find the function and mechanism of miR-34a effect on colon cancer. METHODS: In this study, we examined the expression of miR-34a in colon cancer tissues and cell lines by qRT-PCR. In vitro cell functional assays studies were built to define miR-34a and SYT1 function involved in cell growth, migration, and invasion and apoptosis. EGFP reporter assay was used to determine the relationship of SYT1 and miR-181a. To confirmed the relationship between SYT1 and miR-34a, the SYT1 restoration rescued miR-34a mediated growth and inhibited cell apoptosis were detect. RESULT: Our studies show that microRNA-34a (miR-34a) is downregulated in humancolon cancer relative to normal colon mucosal epithelial cells, and downexpression of miR-34a promotes cell proliferation, migration, and invasion, nevertheless overexpression of miR-34 facilitates cell apoptosis in vitro. Furthermore, SYT1 3'-UTR is found to be down-regulated directly by miR-34a, demonstrating that SYT1 is a important target of miR-34a in colon cancer. The knockdown of SYT1 markedly inhibits colon cancer cell proliferation, migration, and invasion, and induces cell apoptosis, indicating that SYT1 may function as an oncogene in colon cancer. The restoration of SYT1 expression can counteract the effect of miR-34a on cell proliferation, and induces cell apoptosis, of colon cancer cells. CONCLUSION: Together, these results indicate that miR-34a is a new regulator of SYT1, and both miR-34a and SYT1 play the important roles in the pathogenesis of colon cancer. IJCEP
Authors: Helena Nord; Christian Hartmann; Robin Andersson; Uwe Menzel; Susan Pfeifer; Arkadiusz Piotrowski; Adam Bogdan; Wojciech Kloc; Johanna Sandgren; Tommie Olofsson; Göran Hesselager; Erik Blomquist; Jan Komorowski; Andreas von Deimling; Carl E G Bruder; Jan P Dumanski; Teresita Díaz de Ståhl Journal: Neuro Oncol Date: 2009-12 Impact factor: 12.300