Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

PSAT1 prompted cell proliferation and inhibited cell apoptosis in multiple myeloma through regulating PI3K/AKT pathway

Hongqing Zhu^1,2, Yejun Si², Yun Zhuang², Meng Li², Jianmin Ji³, Ou Ji^2,3, Qun Shen^2,3

¹Department of Hematology, Taizhou Hospital Affiliated to Nanjing University of Chinese Medicine, Taizhou City, Jiangsu Province 225300; ²Nanjing University of Chinese Medicine, Nanjing City, Jiangsu Province 210046; ³Department of Hematology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing City, Jiangsu Province 210029, China.

For correspondence:- Qun Shen Email: QunShenkll@126.com Tel:+862586059194

Accepted: 4 February 2020 Published: 29 April 2020

Citation: Zhu H, Si Y, Zhuang Y, Li M, Ji J, Ji O, et al. PSAT1 prompted cell proliferation and inhibited cell apoptosis in multiple myeloma through regulating PI3K/AKT pathway. Trop J Pharm Res 2020; 19(4):745-749 doi: 10.4314/tjpr.v19i4.10

© 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: To identify the biological function of phosphoserine aminotransferase 1 (PSAT1) in regulating cell proliferation and apoptosis in multiple myeloma (MM).

Methods: The mRNA and protein levels of PSAT1 were determined using quantitative real-time polymerase chain reaction (PCR) and western blotting, respectively. Cell proliferation was measured using CCK-8 assay.

Results: PSAT1 mRNA and protein expression levels were significantly increased in MM cell lines when compared to control cells. Moreover, downregulation of PSAT1 inhibited MM cell proliferation and induced cell apoptosis, whereas overexpression of PSAT1 promoted MM cell proliferation and suppressed cell apoptosis. Further analysis demonstrated that the underlying mechanism was via regulation of PI3K/AKT pathway.

Conclusion: The results identified a novel role for PSAT1 in the progression of MM, which may provide a therapeutic and a new anticancer target for the therapy of MM.

Keywords: Multiple myeloma, PSAT1, Cell proliferation, PI3K/AKT pathway