scholarly journals Pyruvate kinase type M2 contributes to the development of pancreatic ductal adenocarcinoma by regulating the production of metabolites and reactive oxygen species

2018 ◽  
Author(s):  
Misa Yokoyama ◽  
Nobuhiro Tanuma ◽  
Rie Shibuya ◽  
Takeharu Shiroki ◽  
Makoto Abue ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Pyruvate Kinase ◽  
Reactive Oxygen ◽  
Ductal Adenocarcinoma ◽  
Oxygen Species

scholarly journals SALL4 suppresses reactive oxygen species in pancreatic ductal adenocarcinoma phenotype via FoxM1/Prx III axis

2018 ◽  
Vol 503 (4) ◽  
pp. 2248-2254 ◽  
Author(s):  
Do Luong Huynh ◽  
Jiao Jiao Zhang ◽  
Nisansala Chandimali ◽  
Mrinmoy Ghosh ◽  
Meeta Gera ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Reactive Oxygen ◽  
Ductal Adenocarcinoma ◽  
Oxygen Species

scholarly journals Insulin Regulates Glucose Consumption and Lactate Production through Reactive Oxygen Species and Pyruvate Kinase M2

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Qi Li ◽  
Xue Liu ◽  
Yu Yin ◽  
Ji-Tai Zheng ◽  
Cheng-Fei Jiang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Liver Cancer ◽  
Pyruvate Kinase ◽  
Molecular Mechanisms ◽  
Cancer Metabolism ◽  
Lactate Production ◽  
Reactive Oxygen ◽  
Glucose Consumption ◽  
Oxygen Species ◽  
Pyruvate Kinase M2

Although insulin is known to regulate glucose metabolism and closely associate with liver cancer, the molecular mechanisms still remain to be elucidated. In this study, we attempt to understand the mechanism of insulin in promotion of liver cancer metabolism. We found that insulin increased pyruvate kinase M2 (PKM2) expression through reactive oxygen species (ROS) for regulating glucose consumption and lactate production, key process of glycolysis in hepatocellular carcinoma HepG2 and Bel7402 cells. Interestingly, insulin-induced ROS was found responsible for the suppression of miR-145 and miR-128, and forced expression of either miR-145 or miR-128 was sufficient to abolish insulin-induced PKM2 expression. Furthermore, the knockdown of PKM2 expression also inhibited cancer cell growth and insulin-induced glucose consumption and lactate production, suggesting that PKM2 is a functional downstream effecter of insulin. Taken together, this study would provide a new insight into the mechanism of insulin-induced glycolysis.

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