Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

MicroRNA miR-103a-3p targets NPAS3 to regulate progression of Alzheimer disease

Yani Zhang¹, Jingjian Wang², Xiaojuan Liu¹, Jiexing Li¹, Shujie Fan¹

For correspondence:- Shujie Fan Email: shujif@outlook.com Tel:+8613627313472

Accepted: 14 Mar 2020 Published: 31 May 2020

Citation: Zhang Y, Wang J, Liu X, Li J, Fan S. MicroRNA miR-103a-3p targets NPAS3 to regulate progression of Alzheimer disease. Trop J Pharm Res 2020; 19(5):1015-1021 doi: 10.4314/tjpr.v19i5.16

© 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: This study aimed at investigating miR-103a-3p expression, functional roles and underlying mechanism in regulating Alzheimer’s progression.

Methods: RT-qPCR was used to assessed miR-103a-3p and NPAS3 expression in human neuroblastoma cells. Cell transfection of overexpressed or knocked down genes and CCK-8 assay measured cell viability while RT-qPCR was used to detect proliferation and apoptosis in biomarkers, Ki87 and PCNA, caspase-8 and caspase-3, respectively. Furthermore, luciferase assay was used to evaluate the luciferase activity while western blotting analysis was applied to determine protein biomarkers regarding proliferation and apoptosis.

Results: expression of miR-103a-3p decreased but NPAS3 increased in AD cell lines. Overexpressed miR-103a-3p attenuated cell viability and NPAS3 bound miR-103a-3p to regulate AD progression. The inhibitory effect of miRNA on cell viability in AD was reversed by NPAS3.

Conclusion: miR-103a-3p/NPAS3 might help to enrich knowledge on treatment of AD.

Keywords: Alzheimer’s development, cell growth, cell proliferation