Overexpression of Vascular Endothelial Growth Factor (VEGF) has been associated with increased angiogenesis, tumor growth and metastasis in tumors. Fibroblast Growth Factor Receptor 3 (FGFR3) acts as an oncogene in several tumor types, including multiple myeloma, bladder cancer and cervical cancer. Our previous studies have shown that inhibition of FGFR3 caused down regulation of VEGF in multiple myeloma. In order to better understand the molecular mechanism of FGFR3 and VEGF, L6 cells lacking any endogenous FGFR were stably transfected with FGFR3 at the present study. The FGFR3 expression was validated by Northern blot and Western blot. Compared with parental L6 cell and L6V (transfected with vector only), L6 cells with stably transfected FGFR3 showed overexpression of VEGF. [3H] Thymidine uptake and CellTiter 96 Aqueous One Solution cell proliferation assay demonstrated that DNA synthesis and cell proliferation were increased in FGFR3 expression L6 cells. These observations indicate that FGFR3 might be associated with regulation of VEGF, suggesting that combinations of inhibition of VEGF and inhibition of FGFR3 may have an advantage for the treatment of FGFR3 overexpression neoplastic disease.
- Fibroblast Growth Factor Receptor 3 (FGFR3)
- L6 cell line
- Vascular Endothelial Growth Factor (VEGF)
ASJC Scopus subject areas