Article Abstract

MicroRNA-374b inhibits the tumor growth and promotes apoptosis in non-small cell lung cancer tissue through the p38/ERK signaling pathway by targeting JAM-2

Authors: Yujun Wang, Lijuan Yu, Tao Wang

Abstract

Background: MicroRNAs (miRNAs) are reportedly involved in various cancers. The present study aimed to investigate the role of miRNA-374b in cell viability, proliferation, apoptosis, and tumor formation in nonsmall cell lung cancer (NSCLC) in humans.
Methods: The expression level of miRNA-374b in blood and tumor tissues from NSCLC patients was analyzed by quantitative reverse transcription polymerase chain reaction (qRT-PCR). A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was performed to assess the viability of NSCLC cells after transfection with miRNA-374b. Colony formation assay was performed to assess the proliferation of cells pretreated with miRNA-374b. The terminal deoxynucleotidyl transferasedUTP nick-end labeling (TUNEL) assay was performed to determine the role of miRNA-374b in apoptosis in NSCLC cells. A tumor formation assay was performed to assess the effects of miRNA-374b on tumorigenesis in NSCLC.
Results: miRNA-374b was markedly downregulated in the blood and tumor tissues from NSCLC patients. Furthermore, overexpression of miRNA-374b markedly reduced the viability of NSCLC cells, but miRNA- 374b inhibitor increased the viability of NSCLC cells compared with that in negative controls. Moreover, miRNA-374b decreased the number of colonies; however, its corresponding anti-miRNA oligonucleotide (AMO) markedly increased colony formation by NSCLC cells. Also, miRNA-374b promoted the apoptosis and inhibited tumor formation in NSCLC; however, this inhibition was reversed upon treatment with the AMO. Western blot analysis revealed that miRNA-374b regulates tumor progression through the p38/ERK signaling pathway by inhibiting JAM-2 in NSCLC.
Conclusions: The present results indicate that miRNA-374b inhibits tumor growth and promotes apoptosis in NSCLC through the p38/ERK signaling pathway by targeting JAM-2.