<b>Results:</b> FGF5 was significantly upregulated in OS tissues and cells, and closely associated with poor differentiation, larger tumor size, lymph node metastasis, and advanced TNM stage.
BC patients in the FGF5 low-expression group were correlated with better clinical characteristics, including tumor size, histopathological grading, estrogen receptors, clinical risk group according to St Gallen criteria, NPI criteria and Veridex signature, DMFS, TDM, and DFS compared with those in the FGF5 high-expression cohort.
Taken together, our data indicated that miR-567 may function as a tumor suppressor by negatively regulating FGF5 and be potential therapeutic targets for the treatment of OS.
In an <i>in vivo</i> experiment in immunocompromised mice, human melanoma xenografts overexpressing FGF5 showed enhanced tumor growth, a higher Ki-67 proliferation index, decreased apoptosis and enhanced angiogenesis.
Two secreted factors whose roles in the constitutive activation of NFkappaB are not well defined were investigated further as pure proteins: transforming growth factor beta2 (TGFbeta2) and fibroblast growth factor 5 (FGF5) were both highly expressed in some mutant clones and tumor cell lines, each activated NFkappaB alone, and the combination was synergistic.