Effects of GSK-3β inhibitor on proliferation and apoptosis of SW480 cells |
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| Authors: | LIU Kun-ping ZHONG Xue-yun LUO Feng ZHAO Tong |
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| Institution: | 1. Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China;
2. Department of Pathology, Qingyuan Hospital, School of Medicine, Jinan University, Qingyuan 511500, China;
3. Department of Pathology, School of Medicine, Jinan University, Guangzhou 510632, China |
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| Abstract: | AIM: To investigate the mechanism and the effect of glycogen synthase kinase 3β (GSK-3β) inhibitor (2’Z,3'E)-6-bromoindirubin-3'-oxime (BIO) on the protein expression of β-catenin and Bcl-2, and proliferation and apoptosis in colon carcinoma SW480 cells.METHODS: The immunohistochemical staining and Western blotting were performed to detect the protein expression of β-catenin, cyclin D1 and Bcl-2. The cell cycle distribution and apoptotic rate were detected by flow cytometry. The morphologic features of SW480 cells before and 24 h after BIO exposure at different concentrations were observed under microscope with HE staining.RESULTS: Compared with the untreated SW480 cells, the protein expression of β-catenin significantly increased and some β-catenin positive nuclear staining positive cells appeared in BIO treated cells. and The cells exposed to BIO showed that the cyclin D1 protein and the cells in S stage and G2/M stage moderately increased, the protein level of Bcl-2 moderately decreased, and the cell apoptosis rate was significantly lower than those in control cells. Furthermore, the morphological changes of the SW480 cells were observed 24 h after BIO treatment. CONCLUSION: Our results indicate that GSK-3β inhibitor BIO participates in the cellular processes of promoting proliferation and inhibiting apoptosis in colon carcinoma cells. The mechanisms are mainly associated with activating the β-catenin pathway and regulating the balance of Bcl-2 pathway, and the up-regulation of β-catenin is most likely the possible factor for SW480 cell regression. |
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| Keywords: | Colorectal neoplasms Glycogen synthase kimase 3β β-catenin Bcl-2 Cell proliferation Apoptosis |
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