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TPI-1通过糖酵解重编程促进胃癌细胞增殖和侵袭的机制

王海伟 张小辉 田云霄 吴士茜

昆明医科大学学报2026,Vol.47Issue(2):35-42,8.
昆明医科大学学报2026,Vol.47Issue(2):35-42,8.DOI:10.12259/j.issn.2095-610X.S20260204

TPI-1通过糖酵解重编程促进胃癌细胞增殖和侵袭的机制

Mechanism of TPI-1 in Promoting the Proliferation and Invasion of Gastric Cancer Cells through Glycolytic Reprogramming

王海伟 1张小辉 1田云霄 1吴士茜1

作者信息

  • 1. 邯郸市中心医院病理科,河北 邯郸 056000
  • 折叠

摘要

Abstract

Objective To investigate the potential mechanism of TPI-1 intervention in gastric cancer progression from the perspective of glycolytic reprogramming.Methods TPI-1 knockdown and overexpression gastric cancer cell models were constructed.Experimental cells were divided into four groups:shCtrl,shTPI-1,oe-Ctrl,and oe-TPI-1.Cell viability was detected using the CCK-8 assay;invasive capacity was assessed using the Transwell assay;glycolytic capacity was measured using glycolytic stress test to detect ECAR reflecting the glycolytic capacity of different groups of gastric cancer cells;Western blot was used to analyze the expression levels of apoptosis-related,invasion-related,and glycolysis-related characteristic markers in different groups;immunofluorescence and co-IP experiments were performed to verify the colocalization and binding relationship between TPI-1 and HK2.Results Compared with the shCtrl group,the shTPI-1 group showed reduced cell proliferation and invasion capacity(P<0.01);compared with the oe-Ctrl group,the oe-TPI-1 group demonstrated enhanced proliferation and invasion capacity(P<0.01);after TPI-1 knockdown,both basal glycolytic capacity and maximum glycolytic capacity were decreased(P<0.01);in the shTPI-1 group,protein levels of glycolytic key enzymes HK2 and PKM2 were significantly reduced(P<0.01),and MMP-2,MMP-9,N-cadherin,Bcl-2,and COX4I1 were significantly downregulated(P<0.01),while NOX4,E-cadherin,Bax,and cleaved caspase-3 were significantly upregulated(P<0.01);the oe-TPI-1 group showed opposite trends;immunofluorescence analysis revealed colocalization of TPI-1 and HK2 within cells;co-immunoprecipitation preliminarily confirmed that TPI-1 and HK2 may interact.Conclusion TPI-1 promotes gastric cancer progression by interacting with HK2,continuously activating the initiation step of glycolysis,and promoting glycolysis reprogramming.

关键词

磷酸丙糖异构酶1/HK2/糖酵解/ECAR/能量代谢/胃癌

Key words

TPI-1/HK2/Glycolysis/ECAR/Energy metabolism/Gastric cancer

分类

医药卫生

引用本文复制引用

王海伟,张小辉,田云霄,吴士茜..TPI-1通过糖酵解重编程促进胃癌细胞增殖和侵袭的机制[J].昆明医科大学学报,2026,47(2):35-42,8.

基金项目

河北省医学科学研究课题计划(20211576) (20211576)

昆明医科大学学报

1003-4706

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