LncRNA colorectal neoplasia differentially expressed promotes glycolysis of liver cancer cells by regulating hypoxia-inducible factor 1α

被引:3
|
作者
Tang, Dan [1 ]
Zhao, Lijin [2 ,3 ]
Mu, Rui [2 ]
Ao, Yu [1 ]
Zhang, Xuyang [1 ]
Li, Xiongxiong [1 ]
机构
[1] Zunyi Med Univ, Affiliated Hosp 2, Dept Hepatopancreatobiliary Surg, Zunyi, Guizhou, Peoples R China
[2] Zunyi Med Univ, Digest Dis Hosp, Affiliated Hosp, Dept Gen Surg, Zunyi, Guizhou, Peoples R China
[3] Zunyi Med Univ, Affiliated Hosp, Dept Hepatopancreatobiliary Surg, 149 Dalian Rd, Zunyi, Guizhou, Peoples R China
来源
CHINESE JOURNAL OF PHYSIOLOGY | 2022年 / 65卷 / 06期
基金
中国国家自然科学基金;
关键词
Colorectal neoplasia differentially expressed; enhancer of zeste homolog 2; glycolysis; hypoxia-inducible factor 1 alpha; liver cancer; miR-142; proliferation;
D O I
10.4103/0304-4920.365458
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
LncRNAs are associated with tumorigenesis of liver cancer. LncRNA Colorectal Neoplasia Differentially Expressed (CRNDE) was identified as an oncogenic lncRNA and involved in tumor growth and metastasis. The role of CRNDE in liver cancer was investigated. CRNDE was elevated in liver cancer cells. Knockdown of CRNDE decreased cell viability and inhibited proliferation of liver cancer. Moreover, knockdown of CRNDE reduced levels of extracellular acidification rate, glucose consumption, and lactate production to repress glycolysis of liver cancer. Silence of CRNDE enhanced the expression of miR-142 and reduced enhancer of zeste homolog 2 (EZH2) and hypoxia-inducible factor 1 alpha (HIF-1 alpha). Over-expression of HIF-1 alpha attenuated CRNDE silence-induced decrease of glucose consumption and lactate production. Injection with sh-CRNDE virus reduced in vivo tumor growth of liver cancer through up-regulation of miR-142 and down-regulation of EZH2 and HIF-1 alpha. In conclusion, knockdown of CRNDE suppressed cell proliferation, glycolysis, and tumor growth of liver cancer through EZH2/miR-142/HIF-1 alpha.
引用
收藏
页码:311 / +
页数:9
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