18β-glycyrrhetinic acid promotes gastric cancer cell autophagy and inhibits proliferation by regulating miR-328-3p/signal transducer and activator of transcription 3

Gastric cancer (GC) is one of the most common cancer types worldwide, and its prevention and treatment methods have garnered much attention. As the active ingredient of licorice, 18β-glycyrrhetinic acid (18β-GRA) has a variety of pharmacological effects. The aim of this study was to explore the effe...

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Published in:World journal of gastroenterology : WJG 2023-07, Vol.29 (27), p.4317-4333
Main Authors: Yang, Yi, Nan, Yi, Du, Yu-Hua, Huang, Shi-Cong, Lu, Dou-Dou, Zhang, Jun-Fei, Li, Xia, Chen, Yan, Zhang, Lei, Yuan, Ling
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Autophagy
Basic Study
Cell Line, Tumor
Cell Proliferation - genetics
Gene Expression Regulation, Neoplastic
Mice
Mice, Nude
MicroRNAs - genetics
MicroRNAs - metabolism
RNA, Messenger
STAT3 Transcription Factor - metabolism
Stomach Neoplasms - drug therapy
Stomach Neoplasms - genetics
Stomach Neoplasms - metabolism
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Summary:Gastric cancer (GC) is one of the most common cancer types worldwide, and its prevention and treatment methods have garnered much attention. As the active ingredient of licorice, 18β-glycyrrhetinic acid (18β-GRA) has a variety of pharmacological effects. The aim of this study was to explore the effective target of 18β-GRA in the treatment of GC, in order to provide effective ideas for the clinical prevention and treatment of GC. To investigate the mechanism of 18β-GRA in inhibiting cell proliferation and promoting autophagy flux in GC cells. Whole transcriptomic analyses were used to analyze and screen differentially expressed microRNAs (miRNAs) in GC cells after 18β-GRA intervention. Lentivirus-transfected GC cells and the Cell Counting Kit-8 were used to detect cell proliferation ability, cell colony formation ability was detected by the clone formation assay, and flow cytometry was used to detect the cell cycle and apoptosis. A nude mouse transplantation tumor model of GC cells was constructed to verify the effect of miR-328-3p overexpression on the tumorigenicity of GC cells. Tumor tissue morphology was observed by hematoxylin and eosin staining, and microtubule-associated protein light chain 3 (LC3) expression was detected by immunohistochemistry. TransmiR, STRING, and miRWalk databases were used to predict the relationship between miR-328-3p and signal transducer and activator of transcription 3 (STAT3)-related information. Expression of mRNA and was detected by quantitative polymerase chain reaction (qPCR) and the expression levels of STAT3, phosphorylated STAT3 (p-STAT3), and LC3 were detected by western blot analysis. The targeted relationship between and was detected using the dual-luciferase reporter gene system. AGS cells were infected with monomeric red fluorescent protein-green fluorescent protein-LC3 adenovirus double label. LC3 was labeled and autophagy flow was observed under a confocal laser microscope. The expression of miR-328-3p was significantly upregulated after 18β-GRA intervention in AGS cells ( = 4.51E-06). Overexpression of miR-328-3p inhibited GC cell proliferation and colony formation ability, arrested the cell cycle in the G0/G1 phase, promoted cell apoptosis, and inhibited the growth of subcutaneous tumors in BALB/c nude mice ( < 0.01). No obvious necrosis was observed in the tumor tissue in the negative control group (no drug intervention or lentivirus transfection) and vector group (the blank vector for lentivirus transfect
ISSN:1007-9327
2219-2840
DOI:10.3748/wjg.v29.i27.4317