文献类型：期刊文献

英文题名：miR-183-5p Promotes HCC Migration/Invasion via Increasing Aerobic Glycolysis

作者：Niu, Yaqian[1];Liu, Fang[1];Wang, Xiuyue[1];Chang, Yuling[1];Song, Yanmei[1];Chu, Huiyuan[1];Bao, Shisan[2,3];Chen, Che[1]

第一作者：Niu, Yaqian

通信作者：Chen, C[1];Bao, SS[2];Bao, SS[3]

机构：[1]Gansu Univ Chinese Med, Sch Publ Hlth, Dept Clin Lab Diagnost, 35 Dingxi East Rd, Lanzhou 730000, Gansu, Peoples R China;[2]Univ Sydney, Fac Med & Hlth, Discipline Pathol, Sch Med Sci, Sydney, NSW 2006, Australia;[3]Univ Sydney, Fac Med & Hlth, Bosch Inst, Charles Perkins Ctr, Sydney, NSW 2006, Australia

第一机构：甘肃中医药大学公共卫生学院

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Sch Publ Hlth, Dept Clin Lab Diagnost, 35 Dingxi East Rd, Lanzhou 730000, Gansu, Peoples R China;[2]corresponding author), Univ Sydney, Fac Med & Hlth, Discipline Pathol, Sch Med Sci, Sydney, NSW 2006, Australia;[3]corresponding author), Univ Sydney, Fac Med & Hlth, Bosch Inst, Charles Perkins Ctr, Sydney, NSW 2006, Australia.|[10735e9d5e7087247e71b]甘肃中医药大学公共卫生学院;[10735]甘肃中医药大学;

年份：2021

卷号：14

起止页码：3649

外文期刊名：ONCOTARGETS AND THERAPY

收录：;Scopus(收录号：2-s2.0-85108539928);WOS:【SCI-EXPANDED(收录号:WOS:000657833000001)】；

基金：This work was supported by Nation's Nature Science Foundation of China (grant no. 81460456), Science evaluation project of Higher education institutions in Gansu Province (2017A-051), Lanzhou Chengguan District Science and Technology Project (2020JSCX0084) and the postgraduate innovation fund project of Gansu University of Chinese Medicine (CX2020-54).

语种：英文

外文关键词：miR-183-5p; aerobic glycolysis; migration; invasion; PTEN/Akt/mTOR; hepatocellular carcinoma

摘要：Background: The mortality and morbidity of hepatocellular carcinoma (HCC) are still unacceptably high, despite decades of extensive studies. Aerobic glycolysis is a hallmark of cancer metabolism, closely relating to invasion and metastasis of HCC. MicroRNAs (miRNAs) are involved in the regulation of aerobic glycolysis. miR-183-5p, an oncogenic miRNA, is highly expressed in HCC, but the regulatory mechanism of miR-183-5p in migration, invasion and aerobic glycolysis in HCC remains unclear. Purpose: To elucidate whether miR-183-5p affects aerobic glycolysis to regulate the migration and invasion of HCC, and to explore its regulatory mechanism. Methods: We attempted to observe the effects of miR-183-5p on the migration and invasion of HepG2 cells by a wound-healing assay and Transwell assays. The effect of miR-183-5p on glycolysis was determined by glucose uptake and lactate generation. Western blot and qPCR were used to detect the relevant proteins and miRNA expression. Results: Our results show that miR-183-5p promoted migration and invasion, enhanced glycolysis via increasing glucose uptake and lactate generation, and up-regulated glycolysis-related gene (PKM2, HK2, LDHA, GLUT1) expression in HepG2 cells. Further experiments indicated that miR-183-5p could decrease PTEN expression, but increased Akt, p-Akt and mTOR expression in HepG2 cells. Conclusion: These findings suggest that miR-183-5p may promote HCC migration and invasion via increasing aerobic glycolysis through targeting PTEN and then activating Akt/ mTOR signaling.