1. [Expression and significance of FGFR2IIIc in chemoresistant bladder cancer cells].
- Author
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Chen Y, Zhang L, Wu K, Zeng J, Gao Y, Wang X, Li H, Chang LS, and He D
- Subjects
- Animals, Cell Transdifferentiation drug effects, Doxorubicin pharmacology, HEK293 Cells, Humans, Neoplasm Metastasis, Protein Isoforms metabolism, Drug Resistance, Neoplasm, Gene Expression Regulation, Neoplastic, Receptor, Fibroblast Growth Factor, Type 2 metabolism, Urinary Bladder Neoplasms metabolism, Urinary Bladder Neoplasms pathology
- Abstract
Objective: To investigate the role of fibroblast growth factor receptor-2 (FGFR2) splice variant FGFR2IIIc in the regulation of mesenchymal-epithelial transition (MET) in doxorubicin-resistant bladder cancer cells., Methods: A doxorubicin-resistant human bladder cell line (253J/DOX) was generated from the bladder cancer cell line 253J by being continuously exposed to gradually increasing doses of doxorubicin. Chemosensitivity to doxorubicin was determined by MTT assay. The expressions of P-glycoprotein and FGFR2IIIc were evaluated by Western blotting and real-time RT-PCR, respectively. Changes in E-cadherin and vimentin were detected by Western blot analysis. Migration ability of 253J and 253J/DOX cells was analyzed by in vitro wound healing assay., Results: The resistant cells, 253J/DOX, were more resistant to doxorubicin than the parent cells. Western blotting and RT-PCR analysis indicated the higher levels of P-glycoprotein and FGFR2IIIc in 253J/DOX cells (P<0.05). Additionally, compared with the 253J cells, 253J/DOX cells presented the upregulation of E-cadherin, the downregulation of vimentin and the inhibition of migration ability., Conclusion: FGFR2IIIc-induced MET in chemoresistant bladder cancer cells may play an important role in the formation of metastatic lesions.
- Published
- 2014