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Archive > Volume 24 Issue 8 > 2017,24(8):880-883. DOI:10.3872/j.issn.1007-385X.2017.08.011 Prev Next
Clinical Research
MicroRNA-99a promotes proliferation and migration of colon cancer cell and its anti-tumor mechanism
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Abstract:
Objective: To investigate the expression of microRNA-99a in the tumor tissues of colon cancer patients and its effect on cancer cell proliferation and migration. Methods: 49 pairs of cancer tissue and adjacent tissue (5 cm away from cancer tissue) from colon cancer patients that treated in Gastrointestinal Center of Affiliated Chang-zhou Second Hospital of Nanjing Medical University, and colon cancer cell lines (HT-29，HCT-116，SW480，Caco-2) as well as normal epithelial HcoePic cell line were selected for our research. Quantitative real-time PCR was used to detect the levels of microRNA-99a in tumor tissues, adjacent tissues and tumor cells; After transfection of mc-iroRNA-99a inhibitor, we used CCK-8 to test the cell proliferation, transwell assay to observe the cell migration,and Western lotting to examine the levels of FGFR3 in HT-29 cells. Results: The expression of microRNA-99a in the cancer tissues was significantly higher than that in normal para-cancerous tissues (6.27±0.48 vs 1.34±0.54, P<0.05), and its expression in tumor cells was significantly higher than that in normal colon epithelial cells（5.48±0.34, 7.67±0.24, 5.78±0.22, 6.28±0.44 vs 1.45±0.37, P<0.05). After microRNA-99a inhibitor transfection, cell pro-liferation and migration of HT-29 cells were significantly decreased (P<0.05); , in the meanwhile, the mRNA and protein levels of FGFR3 were significantly decreased in HT-29 cells (P<0.05). Conclusion: microRNA-99a was highly expressed in the tumor tissue of colon cancer patients and colon cancer cells, and low expression of microR-NA-99a may weaken the proliferation and migration ability of cancer cells, which might be accomplished throughFGFR3 signaling pathway.
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Project Supported:
Project supported by the Changzhou Basic Research Program of Science and Tech-nology （No. CJ20122014）
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