Effects of cell adhesion molecule CD44v6 on the proliferation, apoptosis and migration of bladder cancer cell line T24
10.3781/j.issn.1000-7431.2012.03.005
- Author:
Qian LI
1
Author Information
1. Tianjin Institute of Urology
- Publication Type:Journal Article
- Keywords:
Antigens, CD44v6;
Apoptosis;
Cell proliferation;
Gene expression regulation;
Neoplasm metastasis;
Urinary bladder neoplasms
- From:
Tumor
2012;32(3):177-181
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effect of cell adhesion molecule CD44v6 on biological behavior of bladder cancer cell line T24. Methods: The expressions of CD44v6 protein in bladder transitional epithelial cells and bladder cancer T24 cells were detected by immunocytochemistry. MTT assay was used to detect the growth inhibitory rate of T24 cells treated with different concentrations of anti-CD44v6 monoclonal antibodies for 24, 48 and 72 h, respectively. After T24 cells were treated with anti-CD44v6 monoclonal antibodies, the apoptosis was detected by flow cytometer, the expressions of apoptosis-related markers Bcl-2 and Bax were determined by immunohistochemistry, and the change of migration ability of T24 cells was detected by Transwell migration test. Results: CD44v6 was expressed in T24 cells, but rarely expressed in bladder transitional epithelial cells. MTT assay demonstrated that anti-CD44v6 monoclonal antibodies had inhibitory effects on the proliferation of T24 cells (P <0.01). The apoptosis rate of T24 cells was increased with an induction of anti-CD44v6 monoclonal antibodies (P <0.01). The expression level of Bax protein was up-regulated, while the expression level of Bcl-2 protein was down-regulated in T24 cells (P <0.01). The migration of T24 cells was inhibited after treatment with anti-CD44v6 monoclonal antibodies (P <0.05). Conclusion: Anti- CD44v6 monoclonal antibodies can inhibit the abilities of proliferation and migration of T24 cells, and also induce apoptosis. The mechanism may be related with the expression regulation of Bcl -2 and Bax genes. Copyright© 2012 by TUMOR.
