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Original Research Article | OPEN ACCESS

Isoliquiritigenin inhibits the survival of diffuse large β-cell lymphoma cells by regulating Akt/mTOR signaling pathway

Zhixiang Su1, Bin Yu2 , Zhiping Deng3, Haifeng Sun1

1Department of Medical Oncology Hospital Unit 3; 2Department of Medical Oncology Hospital Unit Chinese Integrative; 3Department of Mastosis Hospital, Shaanxi Province Cancer Hospital, Xi'an City, Shaanxi Province 710061, China.

For correspondence:-  Bin Yu   Email: AZXS073@163.com   Tel:+862985276130

Accepted: 29 July 2020        Published: 31 August 2020

Citation: Su Z, Yu B, Deng Z, Sun H. Isoliquiritigenin inhibits the survival of diffuse large β-cell lymphoma cells by regulating Akt/mTOR signaling pathway. Trop J Pharm Res 2020; 19(8):1619-1623 doi: 10.4314/tjpr.v19i8.8

© 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 investigate the effect of isoliquiritigenin (ISL) on diffuse large B-cell lymphoma (DLBCL) cells and its underlying mechanism of action.
Methods: The DLBCL cell line OCI-Ly19 was used in this study. Cell proliferation was measured by MTT assay. Apoptosis was evaluated using flow cytometry. Phosphorylation of Akt and mTOR was assessed using Western blotting.
Results: DLBCL cell proliferation was suppressed by ISL in a concentration-dependent manner. The number of apoptotic cells increased following ISL treatment in a concentration-dependent manner (p < 0.05). ISL treatment also stopped the cell cycle at the G1 phase in a concentration-dependent manner. Western blot analysis indicated that there was no significant Akt and mTOR expression in cells treated with 10, 20, or 50 µM ISL (p < 0.05). However, Akt and mTOR phosphorylation was upregulated following treatment with 10, 20, or 50 µM ISL in a concentration-dependent manner (p < 0.05).
Conclusion: The results demonstrate that ISL inhibits DLBCL cell proliferation and promotes cell apoptosis by blocking the cell cycle transition from the G1 to S phase, which is mediated by the inactivation of the Akt/mTOR signaling pathway.

Keywords: Isoliquiritigenin, Cell survival, Diffuse large B-cell lymphoma, Akt/mTOR signaling pathway

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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