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Fibroblast growth factor 9 ( FGF 9) promotes cancer progression; however, its role in cell proliferation related to tumorigenesis remains elusive. We investigated how  FGF 9 affected  MA ‐10 mouse Leydig tumor cell proliferation and found that  FGF 9 significantly induced cell proliferation by activating  ERK 1/2 and retinoblastoma (Rb) phosphorylations within 15 minutes. Subsequently, the expressions of E2F1 and the cell cycle regulators: cyclin D1, cyclin E1 and cyclin‐dependent kinase 4 ( CDK 4) in G 1  phase and cyclin A1,  CDK 2 and  CDK 1 in S‐G 2 /M phases were increased at 12 hours after  FGF 9 treatment; and cyclin B1 in G 2 /M phases were induced at 24 hours after  FGF 9 stimulation, whereas the phosphorylations of p53, p21 and p27 were not affected by  FGF 9. Moreover,  FGF 9‐induced effects were inhibited by  MEK  inhibitor  PD 98059, indicating  FGF 9 activated the Rb/E2F pathway to accelerate  MA ‐10 cell proliferation by activating  ERK 1/2. Immunoprecipitation assay and Ch IP ‐quantitative  PCR  results showed that  FGF 9‐induced Rb phosphorylation led to the dissociation of Rb‐E2F1 complexes and thereby enhanced the transactivations of E2F1 target genes,  Cyclin D1, Cyclin E1  and  Cyclin A1 . Silencing of FGF receptor 2 ( FGFR 2) using lentiviral sh RNA  inhibited  FGF 9‐induced  ERK 1/2 phosphorylation and cell proliferation, indicating that  FGFR 2 is the obligate receptor for  FGF 9 to bind and activate the signaling pathway in  MA ‐10 cells. Furthermore, in a severe combined immunodeficiency mouse xenograft model,  FGF 9 significantly promoted  MA ‐10 tumor growth, a consequence of increased cell proliferation and decreased apoptosis. Conclusively,  FGF 9 interacts with  FGFR 2 to activate  ERK 1/2, Rb/E2F1 and cell cycle pathways to induce  MA ‐10 cell proliferation in vitro and tumor growth in vivo.

FGF9/FGFR2 increase cell proliferation by activating ERK 1/2, Rb/E2F1, and cell cycle pathways in mouse Leydig tumor cells