Effect of GSK-3β on proliferation and invasion of endometrioid adenocarcinoma
10.3781/j.issn.1000-7431.2008.04.004
- Author:
Ming-Zhi ZHAO
1
Author Information
1. Department of Gynecology and Obstetrics
- Publication Type:Journal Article
- Keywords:
Cell proliferation;
Endometrial neoplasms;
Glycogen synthase kinase 3;
Neoplasm invasiveness;
RNA;
Small interfering
- From:
Tumor
2008;28(4):288-292
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effects of glycogen synthase kinase-3β(GSK-3β) on the proliferation and invasion abilities of the three cell lines with endometrioid adenocarcinoma Ishikawa, HEC-1A (differentiated) and KLE (undifferentiated). Methods: Three human endometrioid adenocarcinoma cell lines Ishikawa, HEC-1A, and KLE were transfected with GSK-3β siRNA. The expression of GSK-3β protein and apoptosis-related protein caspase-3 were examined by Western blotting. The proliferation of cells transfected with GSK-3β siRNA or negative control siRNA were meausred with BrdU incorporation assay while cell cycle distribution and apoptotic ratio were detected by flow cytometry (FCM). The invasion and migration of cells were tested by Matrigel invasion assay. MMP-2 secretion was assessed by gelatin zymography. Results: The GSK-3β siRNA had high inhibitory effect on the expression of GSK-3β gene. The level of GSK-3β protein was significantly lower in the three cell lines compared with control (P <0.05). Compared with cells transfected with negative control siRNA or non transfected cells, the BrdU incoporation ratio was significantly decreased in Ishikawa and HEC-1-A cells after transfected with GSK-3β siRNA (P <0.05). The proportion of cells in S phase was reduced and the apoptotic rate was increased while the expression of caspase 3 protein was up-regulated and cell invasion ability was down-regulated (P <0.01). But there was no statistical difference in the proliferation and invasion abilities between KLE cells and control (P > 0.05). Conclusion: GSK-3β could promote the proliferation and invasion of the differentiated endometrioid adenocarcinoma cell lines Ishikawa and HEC-1-A, but had no effect on the undifferentiated cell line KLE.
