Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

MiR-148a-3p suppresses the progression of gastric cancer cells through targeting ATP6AP2

Xiaosheng Jin, Peipei Cai, Zhengchao Shi, Fangpeng Ye, Tingting Ji, Rongzhou Li

Ruian People’s Hospital, Ruian City, Zhejiang, China;

For correspondence:- Rongzhou Li Email: lirongzhou@163.com Tel:+8613705781365

Accepted: 30 April 2020 Published: 30 September 2020

Citation: Jin X, Cai P, Shi Z, Ye F, Ji T, Li R. MiR-148a-3p suppresses the progression of gastric cancer cells through targeting ATP6AP2. Trop J Pharm Res 2020; 19(9):1821-1826 doi: 10.4314/tjpr.v19i9.4

© 2020 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: Gastric cancer (GC) is one of the most frequent tumors with high mortality rate, worldwide. A proper understanding of the mechanism underlying its progression is required for its diagnosis and development of novel treatment option. MicroRNAs are associated with the development and advancement of different types of cancer, including GC. The current research was aimed at investigating the molecular and biological function of miR-148a-3p in GC development.

Methods: A human normal gastric epithelial cell line, GES-1 (control) as well as four GC cell lines (NUGC-4, SNU-520, STKM-2 and MKN-74) were employed for the study. MiR-148a-3p and ATP6AP2 expression levels in GC cell lines were examined by RT-qPCR technique. Transfection procedure was used to upregulate miR-148a-3p expression in the MKN-45 cell line. MTT assay was utilized to evaluate cell viability in GC cell lines. The molecular interaction between miR-148a-3p and ATP6AP2 was predicted using bioinformatics system and the prediction was then validated by luciferase reporter assay.

Results: expression levels of miR-148-3p was low, whilst that of ATP6AP2 was high in GC cell lines. MiR-148a-3p overexpression resulted in the reduction of cell viability in GC cell lines. More so, it was confirmed that miR-148-3p, as a post-transcriptional regulator inhibited ATP6AP2 expression by having a negative association with it in GC cells. More so, ATP6AP2 was found to be a direct target of miR-148a-3p.

Conclusion: Our results revealed that miR-148a-3p plays a crucial function in GC development through targeting ATP6AP2. This finding could be explored in the discovery of new therapeutic approaches for GC treatment.

Keywords: ATP6AP2, Cell viability, Gastric cancer, miR-148a-3p, Progression