FGF2 and neoplasm: In addition, downregulation of miR-15a and miR-16 in CAFs in the prostate cancer microenvironment promoted tumor growth and progression by suppressing the posttranscriptional repression of Fgf-2 and its receptor Fgfr1, which enhance tumor-cell survival, proliferation, and migration by acting on both stromal and tumor cells [50].