NDLI: Glycolysis inhibitor 2-deoxy-D-glucose suppresses carcinogen-induced rat hepatocarcinogenesis by restricting cancer cell metabolism.

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Glycolysis inhibitor 2-deoxy-D-glucose suppresses carcinogen-induced rat hepatocarcinogenesis by restricting cancer cell metabolism.

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Glycolysis inhibitor 2-deoxy-D-glucose suppresses carcinogen-induced rat hepatocarcinogenesis by restricting cancer cell metabolism.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wang, Zhaofa Zhang, Liming Zhang, Dong Sun, Rongsheng Wang, Qingyan Liu, Xinyi
Description	Author Affiliation: Wang Z ( Department of General Surgery, Weihai Second Municipal Hospital, Weihai Women and Children's Hospital, Weihai Hospital Affiliated to Qingdao University, Weihai, Shandong 264200, P.R. China.); Zhang L ( Department of Otorhinolaryngology, Weihaiwei People's Hospital, Weihai, Shandong 264000, P.R. China.); Zhang D ( Department of General Surgery, Huadong Hospital Affiliated to Fudan University, Shanghai 200040, P.R. China.); Sun R ( Department of General Surgery, Weihai Second Municipal Hospital, Weihai Women and Children's Hospital, Weihai Hospital Affiliated to Qingdao University, Weihai, Shandong 264200, P.R. China.); Wang Q ( Department of General Surgery, Weihai Second Municipal Hospital, Weihai Women and Children's Hospital, Weihai Hospital Affiliated to Qingdao University, Weihai, Shandong 264200, P.R. China.); Liu X ( Department of General Surgery, Weihai Second Municipal Hospital, Weihai Women and Children's Hospital, Weihai Hospital Affiliated to Qingdao University, Weihai, Shandong 264200, P.R. China.)
Abstract	The abnormal metabolism of cancer cells is a crucial feature of tumors and provides promising therapeutic targets for cancer treatments. Aerobic glycolysis in cancer cells, termed the Warburg effect, is a highlighted characteristic of cancerspecific metabolism. However, the effect of glycolysis inhibition on hepatocarcinogenesis remains to be elucidated. In the present study, the effects of the glycolysis inhibitor 2deoxyDglucose (2DG) on the Ndiethylnitrosamine (DEN)induced rat hepatocarcinoma model and its underlying mechanisms were investigated. It was observed that 2DG significantly delayed hepatocarcinogenesis and effectively prolonged survival time in the DENtreated rats. The glycolysis inhibitor, 2DG prominently decreased cell proliferation and increased cell apoptosis in the DENinduced rat hepatoma and had no evident impact on the pericarcinomatous liver tissues. Further investigation revealed that 2DG resulted in a reduction of glycolysis products, the compensatory increase of hexokinase 2 expression and a decrease in 6phosphofructo2kinase, pyruvate kinase M2 and lactate dehydrogenase A expression in the hepatoma tissues. The inhibition of glycolysis further suppressed the tricarboxylic acid cycle, fatty acid and cholesterol biosynthesis and ATP production, while it promoted autophagic activation. In addition, the in vitro study demonstrated that hypoxia, an important factor in the tumor microenvironment, may assist in increasing 2DGinduced inhibition of cell viability, cell cycle retardation and the decrease of colony formation ability in hepatoma cells. Taken together, the present results suggested that 2DG may inhibit hepatocarcinogenesis in the DENtreated rats via restricting cancer cell metabolism. This finding provides a promising measure in the prevention and treatment of hepatoma.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	3
Volume Number	11
Language	English
Publisher	Spandidos Publications
Publisher Date	2015-03-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Carcinogens Toxicity Cell Transformation, Neoplastic Chemically Induced Metabolism Deoxyglucose Pharmacology Liver Neoplasms Animals Apoptosis Drug Effects Cell Cycle Cell Line, Tumor Cell Proliferation Cell Survival Glycolysis Anoxia Liver Neoplasms, Experimental Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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