| Literature DB >> 28315172 |
Jianzhang Wu1, Xiaojing Du2, Wulan Li1,3, Yangyang Zhou1,2, Encheng Bai1,2, Yanting Kang1,2, Qiuxiang Chen1,2, Weitao Fu1, Di Yun1, Qing Xu4, Peihong Qiu5, Rong Jin6,7, Yuepiao Cai8, Guang Liang1.
Abstract
Fibroblast growth factor receptor 1 (FGFR1), belonging to receptor tyrosine kinases (RTKs), possesses various biological functions. Over-expression of FGFR1 has been observed in multiple human malignancies. Hence, targeting FGFR1 is an attractive prospect for the advancement of cancer treatment options. Here, we present a novel small molecular FGFR1 inhibitor L16H50, which can inhibit FGFR1 kinase in an ATP-independent manner. It potently inhibits FGFR1-mediated signaling in a gastric cancer cell line, resulting in inhibition of cell growth, survival and migration. It also displays an outstanding anti-tumor activity in a gastric cancer xenograft tumor model by targeting FGFR1 signaling. These results show that L16H50 is a potent non-ATP-competitive FGFR1 inhibitor and may provide strong rationale for its evaluation in gastric cancer patients.Entities:
Keywords: Gastric cancer; Migration; Non-ATP competitive FGFR1 inhibitor; Proliferation; Survival
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Year: 2017 PMID： 28315172 DOI： 10.1007/s10495-017-1361-7
Source DB: PubMed Journal: Apoptosis ISSN： 1360-8185 Impact factor: 4.677