miR-199a通过靶向CTGF抑制结直肠癌细胞增殖和迁移

miR-199a inhibited colorectal cancer proliferation and migration via targeting CTGF

目的旨在探讨miR-199a在结直肠癌(CRC)发生过程中的分子机制。方法用miR-199a模拟物转染至CRC细胞系。通过MTT和Transwell实验鉴定CRC细胞的增殖和迁移能力。Western blot和qRT-PCR检测相关基因的表达水平。双荧光素酶法报告实验鉴定miR-199a与结缔组织生长因子(CTGF)的作用关系。结果 miR-199a在CRC细胞系中下调表达,过表达miR-199a可以显著抑制CRC的上皮间质转化(EMT)和血管生成。CTGF是miR-199a的直接靶点。过表达CTGF可抵消miR-199a对EMT和血管生成的抑制作用。结论 miR-199a通过直接靶向CTGF抑制CRC细胞的EMT和血管生成。

Objective microRNAs are expressed abnormally in colorectal cancer (CRC) and could participate in its development. In the study, we aimed to explore the molecular mechanisms of miR-199a in the genesis of CRC. Methods CRC cell lines were transfected with miR-199a mimics. Proliferation and migration were identified by MTT assay and Transwell assay, respectively. Protein and mRNA expression levels of associated genes were measured by Western blot and qRT-PCR, respectively. Dual luciferase assay was used to determine the relation of miR-199a and CTGF. Results miR-199a was down-regulated in CRC cell lines and over expression of miR-199a significantly inhibited EMT and angiogenesis. CTGF was a direct target of miR-199a. Up regulation of CTGF level sufficiently reversed the suppression effects of miR-199a on EMT and angiogenesis. Conclusion miR-199a directly targets CTGF and inhibits its expression, leading to suppression on EMT and angiogenesis of CRC cells. miR-199a might be used as potential therapeutic strategy for CRC treatment.