Open AccessKnockdown of miR‑935 increases paclitaxel sensitivity via regulation of SOX7 in non‑small‑cell lung cancer
Author(s) -
Bing Peng,
Chao Li,
Peng Cai,
Liuyang Yu,
Bolin Zhao,
Guiming Chen
Publication year - 2018
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2018.9330
Subject(s) - paclitaxel , protein kinase b , cancer research , gene knockdown , a549 cell , microrna , oncogene , apoptosis , biology , lung cancer , downregulation and upregulation , cell cycle , cell growth , cancer , chemistry , medicine , biochemistry , genetics , gene
Sex determining region Y‑box (SOX)7 is a member of the SOX family and is responsible for various developmental processes. As a tumor suppressor, decreased expression of SOX7 has been observed in several cancer types, including non‑small‑cell lung cancer (NSCLC). However, the mechanism underlying SOX7 downregulation and its role in chemoresistance in NSCLC remains poorly understood. In the present study, the inhibition of microRNA (miR)‑935 increased the expression of SOX7 at the mRNA and protein levels in A549 cells. The luciferase reporter assay verified that miR‑935 could directly bind to the 3'untranslated region of SOX7 mRNA to suppress its expression in A549 cells. In addition, the inhibition of miR‑935 enhanced the anticancer effect of paclitaxel, i.e., induced cell growth arrest and apoptosis in A549 cells. It was further observed that the inhibition of miR‑935 decreased the B cell lymphoma (Bcl)‑2 and phosphorylated‑RAC‑α serine/threonine‑protein kinase (AKT) protein levels and increased the Bcl‑2 associated X, apoptosis regulator protein levels, without affecting the AKT levels in the presence of paclitaxel within A549 cells. The findings of the present study validate miR‑935 as a predictor of paclitaxel sensitivity in NSCLC.