ESTROGENIC GPER SIGNALING PROMOTES FGF2/FGFR1 ACTIVATION BETWEEN BREAST CANCER-ASSOCIATED FIBROBLASTS (CAFS) AND TUMOR CELLS

M.F. SANTOLLA, , A. VIVACQUA, M. MAGGIOLINI

Article ID: 6472
Vol 32, Issue 4S1, 2018
DOI: https://doi.org/10.54517/jbrha6472
Received: 8 September 2018; Accepted: 8 September 2018; Available online: 8 September 2018; Issue release: 8 September 2018

Abstract

Many cancers acquire aberrant growth and invasion capacity through the dysregulation of fibroblastgrowth factors (FGFs)-mediated signaling (Carter EP, Trends Cell Biol. 2015). In particular, FGFs secretedby the tumor cells or stromal compartment activate the cognate receptors leading to cancer progression(Babina IS, Nat Rev Cancer. 2017). For instance, FGF2-FGFR1 autocrine and/or paracrine loop activationhas been involved in the migration and invasion of cancer cells (Coleman SJ, EMBO Mol. Med. 2014).Remarkably, estrogens induced via the estrogen receptor (ER) the up-regulation and secretion of FGF2in breast and lung cancer (Fillmore CM, PNAS. 2010, Siegfried JM, Oncotarget. 2017). Likewise, the Gprotein estrogen receptor (GPER) was also involved in the regulation of FGF2 by estrogens toward theactivation of downstream signaling pathways in astroglial cells (Huang C, Neuroscience. 2016).



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