Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

MiR-489 serves as a tumor inhibitor in pituitary prolactinoma targeting p21-activated kinase 3

Lie Zhang¹, Shuchuan Miao¹, Zhongxin Yang¹, Zongxi Li¹, Qun Zheng²

¹Department of Neurosurgery, The First Affiliated Hospital of Chengdu Medical College, 610500; ²Department of Health Management Physical Examination Center, Chengdu Fifth People's Hospital, Chengdu City, Sichuan Province 611130, China.

For correspondence:- Qun Zheng Email: zhengqun1207@163.com Tel:+8602882726515

Accepted: 6 March 2021 Published: 31 March 2021

Citation: Zhang L, Miao S, Yang Z, Li Z, Zheng Q. MiR-489 serves as a tumor inhibitor in pituitary prolactinoma targeting p21-activated kinase 3. Trop J Pharm Res 2021; 20(3):559-565 doi: 10.4314/tjpr.v20i3.17

© 2021 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: To evaluate the effect of microRNA-489 (miR-489) on pituitary prolactinoma and its mechanisms of action.

Methods: MMQ and GH3 cells were transfected with miR-489, cell viability assessed with cell counting kit-8 (CCK-8), and clone spots was evaluated by colony formation assay. Transwell assay was applied to measure cell migration and invasion while TargetScan was employed to the presumed targets of miR-489, followed by luciferase reporter assays. was MiR-489 and p21-activated kinase 3 (PAK3) gene expression were determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR. Protein levels of PAK3 were measured using western blots.

Results: Transfection significantly increased miRNA-489 levels (p < 0.01). Cell viability, number of clone spots, as well as cell migration and invasion diminished in MMQ and GH3 cells following miR-489 transfection when compared to miR-NC mimic group (p < 0.01). The presumed binding site of miRNA-489 was located in 3′-untranslated region (UTR) of PAK3, and miR-489 transfection repressed luciferase activity with the wild-type 3′-UTR (p < 0.05). In addition, miR-489 decreased PAK3 levels in MMQ and GH3 cells. Knockdown of PAK3 significantly suppressed cell viability, clone formation ability, as well as cell migration and invasion when compared to negative control (p < 0.01).

Conclusion: MiR-489 overexpression suppresses pituitary prolactinoma by targeting PAK3, thus providing a potential therapeutic strategy for the management of pituitary prolactinoma.

Keywords: Pituitary prolactinoma, MicroRNAs, P21-activated kinase 3