Open AccessMicroRNA-148a inhibits the proliferation and promotes the paclitaxel-induced apoptosis of ovarian cancer cells by targeting PDIA3
Author(s) -
Shuzhen Zhao,
Zhiyuan Wen,
Shanshan Liu,
Ying Liu,
Xiaorui Li,
Yanna Ge,
Shaoru Li
Publication year - 2015
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.2015.3826
Subject(s) - ovarian cancer , microrna , biology , oncogene , apoptosis , gene knockdown , cancer research , paclitaxel , cell growth , cell cycle , microbiology and biotechnology , cancer , gene , biochemistry , genetics
MicroRNAs (miRs) are a class of non-coding RNAs that function as key regulators of gene expression at the post-transcriptional level. miR-148a has been suggested to be associated with human ovarian cancer, however, the detailed functions of miR‑148a in ovarian cancer remain to be fully elucidated. The present study aimed to investigate the regulatory mechanism of miR-148a in ovarian cancer cells. Reverse transcription‑quantitative polymerase chain reaction and western blot analysis were conducted to examine the RNA and protein levels, respectively. The luciferase reporter assay was used to determine the target relationship. Cell proliferation and apoptosis assays were additionally conducted. The present study demonstrated that miR‑148a inhibited cell proliferation and promoted the paclitaxel‑induced apoptosis of ovarian cancer cells. Furthermore, protein disulfide isomerase family A, member 3 (PDIA3) was identified as a target gene of miR‑148a. A fluorescent reporter assay was performed to confirm that miR‑148a was able to directly bind to the 3'‑untranslated region of PDIA3 mRNA. In addition, miR‑148a was frequently downregulated in ovarian cancer tissue, whereas the expression levels of PDIA3 were increased. Knockdown of PDIA3 significantly inhibited the proliferation and promoted the paclitaxel‑induced apoptosis of the ovarian cancer cells, whereas overexpression of PDIA3 had the opposite effects. Therefore, the results of the present study suggested that miR‑148a inhibited the proliferation and promoted the paclitaxel‑induced apoptosis of ovarian cancer cells, and this may be partly attributed to direct targeting of PDIA3.