Basic fibroblast growth factor induces VEGF expression in chondrosarcoma cells and subsequently promotes endothelial progenitor cells-primed angiogenesis

Chondrosarcoma, a common malignant tumor, develops in bone. Effective adjuvant therapy remains inadequate for treatment, meaning poor prognosis. It is imperative to explore novel remedies. Angiogenesis is a rate-limiting step in progression that explains neovessel formation for blood supply in tumor microenvironment. Numerous studies indicate endothelial progenitor cells (EPCs) promoting angiogenesis and contributing to tumor growth. Basic fibroblast growth factor (bFGF), a secreted cytokine, regulates biological activity including angiogenesis and correlates with tumorigenesis. However, the role of bFGF in angiogenesis-related tumor progression by recruiting EPCs in human chondrosarcoma is rarely discussed. Here, we found bFGF induced vascular endothelial growth factor (VEGF) expression via FGFR1/c-Src/p38/NF-κB signaling pathway in chondrosarcoma cells, thereby triggering angiogenesis of endothelial progenitor cells. Our in vivo data revealed tumor-secreted bFGF promoting angiogenesis in both mouse plug and chick chorioallantoic membrane assay (CAM). Xenograft mouse model data, due to bFGF-regulated angiogenesis, showed bFGF regulating angiogenesis-linked tumor growth. Finally, bFGF was highly expressed in chondrosarcoma patients than normal cartilage, positively correlating with VEGF expression and tumor stage. Our study offers a novel therapeutic target for chondrosarcoma progression.

Source: Clinical Science - March 4, 2015 Category: Biomedical Science Authors: H Tzeng, P Chen, K Lin, C Lin, C Tsai, S Han, C Teng, W Hwang, S Wang, C Tang Source Type: research