MicroRNA‐374b inhibits cervical cancer cell proliferation and induces apoptosis through the p38/ERK signaling pathway by binding to JAM‐2

• Published in: Journal of cellular physiology Vol. 233; no. 9; pp. 7379 - 7390
• Main Authors: Li, Guang‐Cai, Cao, Xiao‐Yun, Li, Ying‐Ni, Qiu, Yu‐ Yan, Li, Ying‐Na, Liu, Xing‐Jie, Sun, Xiang‐Xiu
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01-09-2018
• Subjects: Apoptosis; Binding; Cancer; Cell growth; Cell migration; Cell proliferation; Cervical cancer; Cervix; Extracellular signal-regulated kinase; Flow cytometry; Inhibitors; junctional adhesion molecule‐2; Low level; MicroRNAs; migration; miRNA; miRNA‐374b; p38/ERK signaling pathway; Ribonucleic acid; RNA; Scratch tests; Signal transduction; Signaling; siha cell proliferation; siRNA; Therapeutic applications; siha cell proliferation; junctional adhesion molecule-2; p38/ERK signaling pathway; migration; apoptosis; miRNA-374b; cervical cancer
• ISSN: 0021-9541; 1097-4652
• DOI: 10.1002/jcp.26574

Cervical cancer (CC) remains a highly prevalent cancer and mortality globally among women globally. The aim of the present study was to assess the ability of miR‐374b to regulate CC cells through JAM‐2, whilst exploring whether the underlying mechanism and its relation to the p38/ERK signaling pathway. During the study, microRNA‐374b (miR‐374b) was observed to have been expressed at a low level among CC tissues. Hence, a series of miR‐374b mimics, miR‐374b inhibitors, siRNA against JAM‐2, SB202190 (an inhibitor for p38), and PD98059 (an inhibitor for ERK) were introduced to treat CC Siha cells and normal cervical Ect1/E6E7 cells. MTT, flow cytometry, scratch test, and transwell assays were applied to determine cell viability, apoptosis, migration, and invasion. The inhibitory role of the p38/ERK signaling pathway was observed in the CC cells treated with miR‐374b mimics or siRNA against JAM‐2. miR‐374b mimic exposure was found to reduce cell viability, migration, and invasion, but induce apoptosis. MiR‐374b inhibitor exposure was observed to have induced effects on the CC cells in a contrary manner to those induced by that of the miR‐374b mimics. The key findings of the study demonstrated that miR‐374b significantly inhibits cell proliferation, migration, and invasion through the blockade of the p38/ERK signaling pathway activation, as well as negatively binding to JAM‐2, highlighting its potential as a therapeutic target for CC.
The key findings of the study demonstrated that miR‐374b significantly inhibits cell proliferation, migration, and invasion through the blockade of the p38/ERK signaling pathway activation, as well as negatively binding to JAM‐2, highlighting its potential as a therapeutic target for CC.