Premium
Retracted : Overexpression of miR‐4286 is an unfavorable prognostic marker in individuals with non–small cell lung cancer
Author(s) -
An Xian,
Ge Jiwen,
Guo Huihui,
Mi Huaixue,
Zhou Jinhua,
Liu Yongrui,
Wu Zhilian
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29024
Subject(s) - viability assay , cell cycle , cancer research , apoptosis , biology , cell cycle checkpoint , metastasis , cancer , genetics
Non–small cell lung cancer (NSCLC) is still an unresolved source of tumor‐related death internationally. Current studies have discovered that microRNAs (miRNAs) are associated with diverse cancers development, including NSCLC. Our paper focused on the functional character of miR‐4286 in NSCLC. miR‐4286 level in 68 cases of NSCLC tissues, matched neighboring nontumor tissues and different cancer cell lines were inspected by quantitative reverse transcription polymerase chain reaction (qRT‐PCR). The connection concerning miR‐4286 expression and clinicopathological features of patients with NSCLC were further determined. After knockdown or overexpression of miR‐4286, cell viability, cell cycle, and/or apoptotic cells were examined by 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) and flow cytometry assay, respectively. Moreover, the cell cycle‐ and apoptosis‐related proteins were estimated by qRT‐PCR and Western blot. In comparison with the matched nontumor tissues, miR‐4286 was significantly enhanced in lung malignancy tissues and different cell lines. miR‐4286 expression was related with the tumor‐node‐metastasis stage, lymphatic metastasis, and distant metastasis. Cell viability was ominously weakened by suppression of miR‐4286 in A549 cells, whereas was statistically upregulated by overexpression of miR‐4286 in NCI‐H1299 cells. Additionally, we detected that suppression of miR‐4286 tempted cell cycle arrest in G1 stage and fortified apoptosis in A549 cells. Runx3 was recognized as one target gene of miR‐4286, and the impacts of suppression of miR‐4286 on cell viability and apoptosis were through regulation of Runt‐related transcription factor 3. Our study suggests that miR‐4286 overexpression represents a tumor promoter role in NSCLC cells.