The influence of E-cadherin/β-catenin on the glycolysis effect in PANC-1 cells
10.3969/j.issn.1007-3969.2015.02.001
- VernacularTitle:E-cadherin/β-catenin影响胰腺癌PANC-1细胞糖酵解效应的实验研究
- Author:
Yi QIN
;
Dingkong LIANG
;
Si SHI
;
Shunrong JI
;
Bo ZHANG
;
Wenyan XU
;
Jiang LIU
;
Jin XU
;
Quanxing NI
;
Xianjun YU
- Publication Type:Journal Article
- Keywords:
E-cadherin;
β-catenin;
Sirtuin3;
Glycolysis
- From:China Oncology
2015;(2):81-86
- CountryChina
- Language:Chinese
-
Abstract:
Background and purpose:Lower expression of E-cadherin is associated with metastasis of cancer cells, however, the correlation between E-cadherin and glucose metabolism has seldom been reported. This article studied the correlation between E-cadherin and glycolysis effect in PANC-1 cells.Methods:Through treatment of transforming growth factor β (TGF-β) in PANC-1 cells to decrease E-cadherin expression, knock-down the gene of E-cadherin interaction protein β-catenin, and overexpressing of E-cadherin, the effects of E-cadherin on the glucose uptake and lactate production ability and on the expression of key glycolytic genes were assessed.Results:E-cadherin negatively regulated the glycolytic effect of PANC-1 cells by inhibiting glucose uptake and lactate production (P<0.05). Moreover, E-cadherin interacting partner β-catenin signiifcantly promoted glucose metabolism transformation in PANC-1 cells (P<0.05). Moreover, key glycolysis regulator sirtuin 3 (SIRT3) could lower E-cadherin expression.Conclusion:Lower expression of E-cadherin induced the transformation of glucose metabolism transformation in PANC-1 cells and manipulation of E-cadherin expression level could change the glycolysis effect. Moreover, through maneuver glycolysis process could inhibit high metastatic potential of pancreatic cancer cells.
