miR‑26a inhibits ovarian cancer cell proliferation, migration and invasion by targeting TCF12
Author(s) -
Sainan Gao,
Tingting Bian,
Min Su,
Yifei Liu,
Yuquan Zhang
Publication year - 2019
Publication title -
oncology reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.094
H-Index - 96
eISSN - 1791-2431
pISSN - 1021-335X
DOI - 10.3892/or.2019.7417
Subject(s) - carcinogenesis , cancer research , oncogene , biology , microrna , downregulation and upregulation , ovarian cancer , cell growth , metastasis , cancer , transcription factor , cell cycle , gene , genetics
Epithelial ovarian cancer (OC) is a common cause of death from gynecological tumors. MicroRNAs (miRNAs) may function as either oncogenes or tumor suppressors, playing crucial role not only in tumorigenesis, but also in tumor invasion and metastasis. miR‑26a and transcription factor 12 (TCF12) have been reported to be involved in carcinogenesis, but the regulatory role of miR‑26a/TCF12 in OC remains unknown. The aim of the present study was to investigate the expression profiles of TCF12 and miR‑26a in OC patients and the correlation between TCF12 and miR‑26a expression, and to demonstrate the effects of miR‑26a binding on TCF12, to further reveal the miR‑26a/TCF12 regulatory effects on the proliferation, migration, invasion and apoptosis in OC cells. In the present study, the expression of miR‑26a was found to be low, while TCF12 was highly expressed in OC patient tissues and cell lines, and low miR‑26a expression was statistically significantly correlated with high TCF12 expression. To the best of our knowledge, the present study was the first to demonstrate that TCF12 is a direct target of miR‑26a, and upregulation of miR‑26a resulted in TCF12 inhibition in OC cells. Furthermore, the proliferation, migration and invasion were inhibited and apoptosis was induced by miR‑26a upregulation in OC cells. These results indicated that miR‑26a may act as a tumor suppressor in OC, and TCF12 targeting by miR‑26a may be a new therapeutic strategy for OC.
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