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Original Research Article | OPEN ACCESS

Adiponectin regulates the malignant biological behavior of endometrial cancer cells via AMPK/mTOR signal pathway

Li Jin1, Xiumei Feng2, Dan Luo2

1Department of Gynecology, Jingmen No. 1 People's Hospital, Jingmen; 2Department of Gynecology, Jingmen No. 2 People's Hospital, Jingmen, PR China.

For correspondence:-    

Accepted: 24 April 2021        Published: 31 May 2021

Citation: Jin L, Feng X, Luo D. Adiponectin regulates the malignant biological behavior of endometrial cancer cells via AMPK/mTOR signal pathway. Trop J Pharm Res 2021; 20(5):933-938 doi: 10.4314/tjpr.v20i5.7

© 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 study the mechanism by which adiponectin regulates the malignant biological behavior of endometrial cancer cells.
Methods: RL95-2 cells were cultured and re-suspended in complete medium. A preliminary study showed that adiponectin (20 μg/mL) has the most inhibitory effect on cellular proliferation. The cells were divided into control group, 20 μg/mL adiponectin group, and 20 μg/mL adiponectin + 10 μmol/L AMPK inhibitor group, with 4 repeat wells set up for each group. Cell proliferation, apoptosis, invasion and migration ability, as well as the expression levels of MMP-9, Bcl-2, p-AMPK, p-mTOR and p-4ebp1 were determined using standard procedures.
Results: Cell proliferation was significantly higher in the 20 μg/mL adiponectin group than in the 10 μg/mL adiponectin group (p < 0.05). Relative to the control group, apoptosis and p-AMPK expression level in the 10 μg/mL adiponectin group increased, while cell invasion and migratory potential, as well as expression levels of MMP-9, Bcl-2, p-mTOR and p-4ebp1 declined significantly (p < 0.05). The apoptosis and expression level of p-AMPK in the 20 μg/mL adiponectin + 10 μmol/L AMPK inhibitor group decreased, while cell invasion, migratory ability, and amounts of MMP-9, Bcl-2, p-mTOR and p-4ebp1 were elevated, relative to the 20 μg/mL adiponectin group (p < 0.05).
Conclusion: Adiponectin promotes apoptosis of endometrial cancer cells via AMPK/mTOR signaling pathway, and inhibits cell proliferation, invasion and migration. Thus, adiponectin has the potential to exert anti-tumor effect in humans

Keywords: Adiponectin, AMPK/mTOR, Endometrial cancer, Biological behavior, Mechanism

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

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