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Original Research Article | OPEN ACCESS

AKR1C1 overexpression attenuates the inhibitory effect of glycyrrhizic acid on gastric cancer cell proliferation and migration

Lian Qiao1, Cheng Shi2, Junxia Gao1, Yalei Liu1, Qian Zheng1

1Experimental Center, Hebei University of Chinese Medicine, Shijiazhuang City, Hebei Province 050000, China; 2Department of Clinical Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang City, Hebei Province 050000, China.

For correspondence:-  Qian Zheng   Email: zhengqian920@163.com   Tel:+8631189926205

Accepted: 17 March 2022        Published: 30 April 2022

Citation: Qiao L, Shi C, Gao J, Liu Y, Zheng Q. AKR1C1 overexpression attenuates the inhibitory effect of glycyrrhizic acid on gastric cancer cell proliferation and migration. Trop J Pharm Res 2022; 21(4):707-714 doi: 10.4314/tjpr.v21i4.4

© 2022 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 involvement of aldo-keto reductase family 1 member C1 (AKR1C1) in glycyrrhizic acid-mediated gastric cancer.
Methods: Immunohistochemistry, quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), and western blot were used to assess AKR1C1 expression in gastric cancer. Cell proliferation was assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) and colony formation assay. Apoptosis was evaluated by flow cytometry. Transwell and wound healing assays were performed to investigate cell invasion and migration, respectively.
Results: AKR1C1 was significantly upregulated in gastric cancer tissues and cells (p < 0.01). AKR1C1 knockdown suppressed cell proliferation, migration, and invasion of gastric cancer, but promoted cell apoptosis. Glycyrrhizic acid treatment reduced AKR1C1 expression in gastric cancer cells (p < 0.05). AKR1C1 overexpression attenuated the glycyrrhizic acid-induced increase in gastric cancer cell apoptosis as well as the decrease in cell proliferation, migration, and invasion.
Conclusion: AKR1C1 contributes to gastric cancer cell proliferation and metastasis and counteracts the suppressive effects of glycyrrhizic acid on gastric cancer cell proliferation and metastasis.

Keywords: AKR1C1, Gastric cancer, Proliferation, Metastasis, Glycyrrhizic acid

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

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