malonyl-coenzyme-a and Carcinoma--Hepatocellular

malonyl-coenzyme-a has been researched along with Carcinoma--Hepatocellular* in 1 studies

Other Studies

1 other study(ies) available for malonyl-coenzyme-a and Carcinoma--Hepatocellular

Article	Year
Metabolic reprogramming enables hepatocarcinoma cells to efficiently adapt and survive to a nutrient-restricted microenvironment. Cell cycle (Georgetown, Tex.), 2018, Volume: 17, Issue:7 Hepatocellular carcinoma (HCC) is a metabolically heterogeneous cancer and the use of glucose by HCC cells could impact their tumorigenicity. Dt81Hepa1-6 cells display enhanced tumorigenicity compared to parental Hepa1-6 cells. This increased tumorigenicity could be explained by a metabolic adaptation to more restrictive microenvironments. When cultured at high glucose concentrations, Dt81Hepa1-6 displayed an increased ability to uptake glucose (P<0.001), increased expression of 9 glycolytic genes, greater GTP and ATP (P<0.001), increased expression of 7 fatty acid synthesis-related genes (P<0.01) and higher levels of Acetyl-CoA, Citrate and Malonyl-CoA (P<0.05). Under glucose-restricted conditions, Dt81Hepa1-6 used their stored fatty acids with increased expression of fatty acid oxidation-related genes (P<0.01), decreased triglyceride content (P<0.05) and higher levels of GTP and ATP (P<0.01) leading to improved proliferation (P<0.05). Inhibition of lactate dehydrogenase and aerobic glycolysis with sodium oxamate led to decreased expression of glycolytic genes, reduced lactate, GTP and ATP levels (P<0.01), increased cell doubling time (P<0.001) and reduced fatty acid synthesis. When combined with cisplatin, this inhibition led to lower cell viability and proliferation (P<0.05). This metabolic-induced tumorigenicity was also reflected in human Huh7 cells by a higher glucose uptake and proliferative capacity compared to HepG2 cells (P<0.05). In HCC patients, increased tumoral expression of Glut-1, Hexokinase II and Lactate dehydrogenase correlated with poor survival (P = 2.47E Topics: Acetyl Coenzyme A; Adaptation, Physiological; Animals; Carcinoma, Hepatocellular; Cell Line, Tumor; Cell Proliferation; Cell Survival; Citric Acid; Citric Acid Cycle; Fatty Acids; Gene Expression Regulation, Neoplastic; Glucose; Glucose Transporter Type 1; Glycolysis; Hep G2 Cells; Hexokinase; Humans; L-Lactate Dehydrogenase; Lipid Metabolism; Liver Neoplasms; Malonyl Coenzyme A; Mice; Signal Transduction; Survival Analysis; Triglycerides	2018

Article

Year

Metabolic reprogramming enables hepatocarcinoma cells to efficiently adapt and survive to a nutrient-restricted microenvironment.

Cell cycle (Georgetown, Tex.), 2018, Volume: 17, Issue:7

Hepatocellular carcinoma (HCC) is a metabolically heterogeneous cancer and the use of glucose by HCC cells could impact their tumorigenicity. Dt81Hepa1-6 cells display enhanced tumorigenicity compared to parental Hepa1-6 cells. This increased tumorigenicity could be explained by a metabolic adaptation to more restrictive microenvironments. When cultured at high glucose concentrations, Dt81Hepa1-6 displayed an increased ability to uptake glucose (P<0.001), increased expression of 9 glycolytic genes, greater GTP and ATP (P<0.001), increased expression of 7 fatty acid synthesis-related genes (P<0.01) and higher levels of Acetyl-CoA, Citrate and Malonyl-CoA (P<0.05). Under glucose-restricted conditions, Dt81Hepa1-6 used their stored fatty acids with increased expression of fatty acid oxidation-related genes (P<0.01), decreased triglyceride content (P<0.05) and higher levels of GTP and ATP (P<0.01) leading to improved proliferation (P<0.05). Inhibition of lactate dehydrogenase and aerobic glycolysis with sodium oxamate led to decreased expression of glycolytic genes, reduced lactate, GTP and ATP levels (P<0.01), increased cell doubling time (P<0.001) and reduced fatty acid synthesis. When combined with cisplatin, this inhibition led to lower cell viability and proliferation (P<0.05). This metabolic-induced tumorigenicity was also reflected in human Huh7 cells by a higher glucose uptake and proliferative capacity compared to HepG2 cells (P<0.05). In HCC patients, increased tumoral expression of Glut-1, Hexokinase II and Lactate dehydrogenase correlated with poor survival (P = 2.47E

Topics: Acetyl Coenzyme A; Adaptation, Physiological; Animals; Carcinoma, Hepatocellular; Cell Line, Tumor; Cell Proliferation; Cell Survival; Citric Acid; Citric Acid Cycle; Fatty Acids; Gene Expression Regulation, Neoplastic; Glucose; Glucose Transporter Type 1; Glycolysis; Hep G2 Cells; Hexokinase; Humans; L-Lactate Dehydrogenase; Lipid Metabolism; Liver Neoplasms; Malonyl Coenzyme A; Mice; Signal Transduction; Survival Analysis; Triglycerides

2018