Role and mechanism of XPOT inhibition by atractylenolide I in gastric cancer cells
10.3969/j.issn.1006-5725.2024.14.005
- VernacularTitle:白术内酯Ⅰ在胃癌细胞中抑制输出蛋白T的作用和机制
- Author:
Yi ZHANG
1
;
Fangqi MA
;
Siyuan WEI
;
Xuejun LI
Author Information
1. 安徽中医药大学第二附属医院脾胃科 (合肥 230061)
- Keywords:
atractylodes macrocephala lactone Ⅰ;
gastric cancer;
XPOT;
ubiquitination proteasome pathway
- From:
The Journal of Practical Medicine
2024;40(14):1928-1934
- CountryChina
- Language:Chinese
-
Abstract:
Objective This study aimed to investigate the role and mechanism of atractylenolide Ⅰ in inhibiting XPOT proliferation and invasion in gastric cancer cells.Methods This study included exploration of XPOT expression in gastric cancer tissues,analysis of gene expression data from GC patients in TCGA and GEO databases,as well as various cellular assays to detect the ability of cancer cells to proliferate,migrate,and invade.Protein expression levels of XPOT,SKP2,CyclinA,and P27 mRNA were also detected by qPCR and Western Blot.Results Analysis confirmed that XPOT was highly expressed in gastric cancer tissues,indicating a poor prognosis.In vitro studies revealed that AT-1 inhibits the proliferation and invasion ability of GC cells;XPOT down-regulation also inhibits these abilities.Furthermore,AT-1 down-regulates the expression of XPOT which then regulates SKP2,P27,and CyclinA-ultimately inhibiting the proliferation and invasion of gastric cancer cells through the regulation of the XPOT pathway.Conclusion The overexpression of XPOT in gastric cancer tissues can indicate a poor prognosis.Atractylenolide Ⅰ down-regulates the XPOT-regulated ubiquitination-proteasome pathway to inhibit proliferation and invasion of gastric cancer cells.
