Open AccessmiR‑671‑3p is downregulated in non‑small cell lung cancer and inhibits cancer progression by directly targeting CCND2
Author(s) -
Yuanshan Yao,
Ye Zhou,
Xiaojun Fu
Publication year - 2019
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.2019.9858
Subject(s) - oncogene , cell cycle , microrna , cancer research , cell growth , biology , cancer , lung cancer , cell , a549 cell , downregulation and upregulation , oncology , medicine , gene , genetics
MicroRNAs (miRNAs) are implicated in the development and progression of non‑small cell lung cancer (NSCLC). A previous study suggested that miR‑671‑3p suppresses the development of breast cancer. However, the role of miR‑671‑3p in NSCLC remains largely unknown. In the present study, it was identified that miR‑671‑3p was significantly upregulated in NSCLC tissues compared with adjacent normal tissues by reverse transcription quantitative polymerase chain reaction (RT‑qPCR). Similarly, decreased levels of miR‑671‑3p in NSCLC cell lines were observed compared with those in the non‑tumorigenic human bronchial epithelial NL20 cell line. Cell Counting Kit‑8 and Transwell invasion assays indicated that miR‑671‑3p overexpression suppressed the proliferation and invasion of A549 cells, and vice versa. Mechanistically, it was demonstrated that CCND2 was a direct target of miR‑671‑3p. RT‑qPCR and western blot analysis indicated that miR‑671‑3p overexpression decreased the expression of CCND2 in A549 cells. Furthermore, rescue experiments demonstrated that the restoration of CCND2 may significantly reverse the suppressive roles of miR‑671‑3p overexpression on NSCLC cell proliferation and invasion. Taken together, the present study demonstrated that miR‑671‑3p exerted its tumor‑suppressive roles via directly targeting CCND2 in NSCLC.