期刊
CANCER LETTERS
卷 351, 期 1, 页码 143-150出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2014.05.012
关键词
c-Met; SOMCL-863; Receptor tyrosine kinase; Cancer; Angiogenesis
类别
资金
- National Program on Key Basic Research Project of China [2012CB910704]
- National Natural Science Foundation [91229205, 81102461, 81321092]
- National S&T Major Projects [2012ZX09301001-007]
Deregulation of HGF/c-Met signaling and its driven neoplastic phenotype are associated with a variety of human malignancies. We herein reported SOMCL-863 as a novel selective c-Met inhibitor which effectively abrogated c-Met signaling pathways, thereby leading to substantial impairment of c-Met-dependent cell proliferation, migration, invasion, cell scattering and invasive growth. In EBC-1 and NCI-H1993 xenografts, SOMCL-863 exerted significant anti-tumor efficacy through anti-proliferative effects and antiangiogenic mechanisms, including reduction of tumor cell proliferation and reductions of microvessel density and secretion of proangiogenic factor IL-8. Together with the optimal pharmacokinetic properties, SOMCL-863 is a promising candidate worthy for further evaluation as a treatment of c-Met-driven human cancers. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
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