Department of General Surgery, The First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning 121001, PR China.
Department of General Surgery, Jinzhou Central Hospital, Jinzhou, Liaoning 121001, PR China.
Life Sci. 2016 Jul 15;157:12-18. doi: 10.1016/j.lfs.2016.05.039. Epub 2016 May 31.
MicroRNA-505 (miR-505) expressions have been reported to be altered in the serum of HCC patients. However, the effect and underlying mechanism of miR-505 in hepatoma cells remains poorly understood. The present study intended to investigate the expression levels and the probable role and molecular basis of miR-505 in hepatoma cells.
Real-time PCR was used to determine the miR-505 expressions in hepatoma cell lines QGY-7703, SMMC-7721 and MHCC97. Furthermore, an up-or down-regulation of miR-505 was performed in MHCC97 by transfected with miR-505 mimics or anti-miR-505, respectively. Cell proliferation, cell invasion, and epithelial-mesenchymal transition were determined. Moreover, the target gene of miR-505 was also investigated.
The expressions of miR-505 were down-regulated in three hepatoma cell lines. MHCC97 possessed the lowest miR-505 levels among the three hepatoma cell lines. Furthermore, the up-regulation of miR-505 suppressed, whereas the down-regulation of miR-505 promoted proliferation, invasion and epithelial-mesenchymal transition in MHCC97. Moreover, miR-505 could directly bind to the 3'-untranslated region of High-Mobility Group Box 1. Notably, High-Mobility Group Box 1 knockdown apparently promoted cell proliferation and invasion in MHCC97.
We investigated that MiR-505 regulates proliferation and invasion in MHCC97 cells via targeting High-Mobility Group Box 1.
已有研究报道,微小 RNA-505(miR-505)在肝癌患者的血清中表达发生改变。然而,miR-505 在肝癌细胞中的作用及其潜在机制仍知之甚少。本研究旨在探讨 miR-505 在肝癌细胞中的表达水平及其可能的作用和分子基础。
采用实时 PCR 法检测肝癌细胞系 QGY-7703、SMMC-7721 和 MHCC97 中 miR-505 的表达。然后,通过转染 miR-505 模拟物或抗 miR-505 分别上调或下调 MHCC97 中的 miR-505。检测细胞增殖、细胞侵袭和上皮-间充质转化。此外,还研究了 miR-505 的靶基因。
miR-505 在三种肝癌细胞系中的表达均下调。在这三种肝癌细胞系中,MHCC97 的 miR-505 水平最低。此外,上调 miR-505 抑制,而下调 miR-505 促进 MHCC97 增殖、侵袭和上皮-间充质转化。此外,miR-505 可直接结合高迁移率族蛋白盒 1 的 3'非翻译区。值得注意的是,高迁移率族蛋白盒 1 敲低明显促进 MHCC97 细胞的增殖和侵袭。
我们通过靶向高迁移率族蛋白盒 1 研究了 MiR-505 调节 MHCC97 细胞增殖和侵袭的机制。