Basic fibroblast growth factor regulates proliferation and motility of human hepatoma cells by an autocrine mechanism
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NCAM- and FGF-2-mediated FGFR1 signaling in the tumor microenvironment of esophageal cancer regulates the survival and migration of tumor-associated macrophages and cancer cells
2016, Cancer LettersCitation Excerpt :FGF-2 promotes the chemotaxis and proliferation of endothelial cells through Erk1/2 signaling, resulting in wound repair [48,49]. The autocrine, paracrine and intracrine growth promotion of FGF-2/FGFR1 signaling has been confirmed in various tumors [50–53]. In macrophages, the induction of vasculogenic mimicry formation in multiple myeloma is involved in the promotion of macrophage chemotaxis through an FGF-2/FGFR1 paracrine mechanism [54].
Therapeutic uses of FGFs
2016, Seminars in Cell and Developmental BiologyCitation Excerpt :In vitro studies demonstrate an upregulation of FGF5 in the majority of renal cell, prostate, and breast carcinoma cell lines [35]. The upregulation of FGF8, 17 and 18 occur in HCC [36,37]. In several preclinical models, FGF4, 5, 8 and 18 overexpression appear to promote tumor formation via modulating blood vessel growth by the cross-talk between FGFs, vascular endothelial growth factors (VEGFs), and inflammatory cytokines/chemokines [38].
MTORC1 and FGFR1 signaling in fibrolamellar hepatocellular carcinoma
2015, Modern PathologyThe prognostic significance of vasohibin 1-associated angiogenesis in patients with hepatocellular carcinoma
2014, Human PathologyCitation Excerpt :FGF-2 is also reported to have a direct effect on the proliferation activity of ECs, which was determined by double immunostaining of CD34 and proliferating cell nuclear antigen [28]. In addition, FGF-2 stimulates DNA synthesis and cell motility in tumor cells of HCC in an autocrine manner [29]. These results suggest that FGF-2 secretion may play potent roles in tumor-associated angiogenesis and progression in HCC.
The evolving landscape of therapeutic drug development for hepatocellular carcinoma
2013, Contemporary Clinical TrialsCitation Excerpt :FGF is highly expressed in HCC. It promotes cell proliferation via an autocrine mechanism [39,40] and has been shown to augment the angiogenic effect of VEGF [40]. Although originally identified as a Raf kinase inhibitor, sorafenib's activity in HCC is believed to be due to inhibition of VEGFR [41].
New Opportunities in the Systemic Treatment of Hepatocellular Carcinoma—Today and Tomorrow
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