Department of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.
Oncol Rep. 2017 Dec;38(6):3545-3553. doi: 10.3892/or.2017.6054. Epub 2017 Oct 23.
The present study was designed to assess the expression of microRNA-542-3p (miR-542-3p) in human colon cancer and investigate the possible molecular mechanisms underlying the effect of miR-542-3p on the growth and invasion of colon cancer cells. We found that miR-542-3p expression was downregulated in colon cancer patient tissues, compared with that observed in the control group. Silencing of miR‑542-3p expression significantly promoted cell viability and inhibited apoptosis. In addition, overexpression of miR-542-3p significantly reduced cell viability and promoted apoptosis in colon cancer cells. Meanwhile, silencing of miR-542-3p expression significantly suppressed PI3K and p-AKT and survivin protein expression, while overexpression of miR-542-3p significantly induced PI3K and p-AKT and survivin protein expression in colon cancer cells. PI3K inhibitor (LY294002) or survivin inhibitor (YM155) suppressed PI3K/AKT/survivin signaling and increased the anticancer effects of miR-542-3p on the apoptosis in colon cancer. The present study demonstrated that upregulation of miR-542-3p inhibited the growth and invasion of colon cancer cells through PI3K/AKT/survivin signaling, highlighting a novel therapeutic approach for the treatment of colon cancer.
本研究旨在评估微小 RNA-542-3p（miR-542-3p）在人结肠癌中的表达，并探讨 miR-542-3p 对结肠癌细胞生长和侵袭的影响的可能分子机制。我们发现，与对照组相比，结肠癌患者组织中 miR-542-3p 的表达下调。沉默 miR-542-3p 的表达显著促进了细胞活力并抑制了细胞凋亡。此外，过表达 miR-542-3p 显著降低了结肠癌细胞的活力并促进了细胞凋亡。同时，沉默 miR-542-3p 的表达显著抑制了 PI3K 和 p-AKT 和 survivin 蛋白的表达，而过表达 miR-542-3p 则显著诱导了 PI3K 和 p-AKT 和 survivin 蛋白的表达。PI3K 抑制剂（LY294002）或 survivin 抑制剂（YM155）抑制了 PI3K/AKT/survivin 信号通路，增强了 miR-542-3p 对结肠癌细胞凋亡的抗癌作用。本研究表明，上调 miR-542-3p 通过 PI3K/AKT/survivin 信号通路抑制结肠癌细胞的生长和侵袭，为结肠癌的治疗提供了一种新的治疗方法。
