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

被引:7
|
作者
Qiao, Lian [1 ]
Shi, Cheng [2 ]
Gao, Junxia [1 ]
Liu, Yalei [1 ]
Zheng, Qian [1 ]
机构
[1] Hebei Univ Chinese Med, Expt Ctr, Shijiazhuang, Hebei, Peoples R China
[2] Hebei Univ Chinese Med, Dept Clin Pharm, Shijiazhuang, Hebei, Peoples R China
关键词
Gastric cancer; Proliferation; Metastasis; Glycyrrhizic acid; KETO REDUCTASE 1C1; DRUG-RESISTANCE; CYCLE;
D O I
10.4314/tjpr.v21i4.4
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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.
引用
收藏
页码:707 / 712
页数:6
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