首页|期刊导航|海南医科大学学报|缺氧相关基因FHDC1对肝癌细胞增殖、侵袭转移及糖酵解能力的影响

缺氧相关基因FHDC1对肝癌细胞增殖、侵袭转移及糖酵解能力的影响OA

The effect of hypoxia-related gene FHDC1 on progression,migration,invasion and glycolysis of hepatocellular carcinoma cells

中文摘要英文摘要

目的:分析缺氧相关基因FH2 domain containing 1(FHDC1)对肝细胞癌(hepatocellular carcinoma,HCC)细胞增殖、迁移、侵袭及糖酵解能力的影响.方法:Western blot检测缺氧诱导因子1α(HIF-1α)敲除的人肝癌细胞HepG2中HIF-1α与FHDC1的蛋白表达水平.采用慢病毒感染的方法分别构建稳定过表达和敲除FHDC1的肝癌细胞株HepG2和Hep3B,在常氧和缺氧条件下分别利用CCK-8、平板克隆形成实验、Transwell迁移与侵袭实验检测FHDC1对HepG2和Hep3B细胞增殖、迁移与侵袭能力的影响.Western blot检测常氧与缺氧条件下 FHDC1 对 HepG2 和 Hep3B 细胞糖酵解关键蛋白:葡萄糖转运体 1(glucose transporter 1,GLUT1)、丙酮酸激酶M2(pyruvate kinase M2,PKM2)和乳酸脱氢酶(lactate dehydrogenase,LDHA)表达的影响.结果:常氧及缺氧条件下,FHDC1在HIF-1α敲除的HepG2细胞中表达均下调.常氧及缺氧条件下,与相应对照组比较,FHDC1过表达均可增强肝癌细胞 HepG2和 Hep3B 的增殖、迁移与侵袭能力;而敲除FHDC1后,2种肝癌细胞的增殖、迁移与侵袭能力均降低(P<0.05).常氧及缺氧条件下,FHDC1过表达的HepG2和 Hep3B 细胞中 GLUT1、PKM2和 LDHA 的表达均上升;而在 2种肝癌细胞中敲除 FHDC1后,GLUT1、PKM2和 LDHA 的表达均降低(P<0.05).结论:在肝癌细胞中 HIF-1α可调控 FHDC1的表达,FHDC1能够增强肝癌细胞的增殖、迁移与侵袭能力,并促进肝癌细胞糖酵解相关蛋白的表达.

Objective:To investigate the effects of hypoxia-related gene FH2 domain containing 1(FHDC1)on progression,migration,invasion and glycolysis of hepatocellular carcinoma(HCC)cells.Methods:Western blot was used to detect the protein expression of HIF-1α and FHDC1 in HepG2 cells after hypoxia-inducible factor 1-α(HIF-1α)knocked out.Hepatoma cell lines HepG2 and Hep3B with stable overexpression and knockout of FHDC1 were constructed by lentiviral transfection,respectively.CCK-8,plate colony formation assay,Transwell migration and invasion assay were used to detect the effects of FHDC1 on the proliferation,migration,and invasion of HepG2 and Hep3B cells under normoxia and hypoxia.Western blot was used to investi-gate the effects of FHDC1 under normoxic and hypoxic conditions on the expression of key glycolytic proteins in HepG2 and Hep3B cells:glucose transporter 1(GLUT1),pyruvate kinase M2(PKM2),and lactate dehydrogenase(LDHA).Results:The expression of FHDC1 was downregulated in HepG2 cells with HIF-1α-knockout under normoxia and hypoxia.Whether nor-moxia or hypoxia,compared to the corresponding control groups,overexpression of FHDC1 could enhance the proliferation,mi-gration,and invasion of HepG2 and Hep3B cells.Conversely,the proliferation,migration,and invasion of HepG2 and Hep3B cells were decreased after knockout of FHDC1.Under normoxia and hypoxia,the expressions of GLUT1,PKM2,and LDHA was increased in FHDC1-overexpressed HepG2 and Hep3B cells;While after knockout of FHDC1,the expressions of GLUT1,PKM2,and LDHA was decreased in HepG2 and Hep3B cells(P<0.05).Conclusion:HIF-1α regulates FHDC1 expres-sion in HCC cells.FHDC1,in turn,enhances the proliferation,migration,and invasion of HCC cells,and promotes the expresion of glycolysis-related proteins.

夏会东;梁念孩;杨伟;摆茹

宁夏医科大学基础医学院,宁夏 银川 750004宁夏医科大学基础医学院,宁夏 银川 750004宁夏中西医结合医院,宁夏 银川 750021宁夏医科大学基础医学院,宁夏 银川 750004

医药卫生

肝细胞癌FHDC1缺氧迁移侵袭糖酵解

Hepatocellular carcinomaFHDC1HypoxiaMigrationInvasionGlycolysis

《海南医科大学学报》 2026 (15)

1147-1154,8

This study was supported by the Natural Science Foundation of Ningxia(2023AAC03721) 宁夏自然科学基金(2023AAC03721)

10.13210/j.cnki.jhmu.20250327.002

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