Open AccessmiR-768-3p is involved in the proliferation, invasion and migration of non-small cell lung carcinomas
Author(s) -
Zuozhou Xie,
Weiqiang Chen,
Yinghua Chen,
Xiang Wang,
Wenyong Gao,
Yi Liu
Publication year - 2017
Publication title -
international journal of oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.405
H-Index - 122
ISSN - 1019-6439
DOI - 10.3892/ijo.2017.4133
Subject(s) - antagomir , cancer research , apoptosis , microrna , cell growth , biology , oncogene , transfection , a549 cell , cell cycle , lung cancer , cell , cell culture , medicine , pathology , gene , biochemistry , genetics
Altered microRNA expression has been found to be a common feature of several cancers, including lung carcinomas. However, the possible roles of miR-768-3p in the pathological changes of lung carcinomas are still unknown. The aim of the present study was to investigate the expression and possible effects of miR-768-3p in human non-small cell lung carcinomas (NSCLC). Eighty-three NSCLC patients attending the clinic of Kunming Hospital were invited to participate in the study. Their tumor samples were obtained for qRT-PCR analysis. Human NSCLC cell lines, A549 and HCC4006, were employed and transfected with either miR-768-3p mimics or miR-768-3p antagomir. Following transfection, the in vitro and in vivo proliferation, apoptosis fractions, migration and invasion of NSCLC cells were evaluated. The data revealed that: i) upregulated miR-768-3p in tumors were associated with the clinicopathological features of NSCLC patients; ii) inhibiting miR-768-3p function by miR-768-3p antagomir induced distinctly apoptosis and Fas/FasL expressional alteration of NSCLC cells; iii) miR-768-3p antagomir transduction also decreased the viability, migration and invasion, as well as MMP-2 and MMP-9 activities in A549 and HCC4006 cells; and iv) miR-768-3p antagomir transfection also inhibited the growth and proliferation of NSCLC xenografts in nude mice. The present results suggested that abnormal elevated miR-768-3p in NSCLC tumors and cell lines played important roles in NSCLC carcinogenic progression, and the targeting of miR-768-3p might be a potential therapeutic strategy for the treatment of NSCLC.