期刊
FRONTIERS IN BIOSCIENCE-LANDMARK
卷 13, 期 -, 页码 1857-1865出版社
FRONTIERS IN BIOSCIENCE INC
DOI: 10.2741/2805
关键词
EGFR transactivation; GPCR crosstalk; review
资金
- NATIONAL CANCER INSTITUTE [R01CA098372, P50CA097190] Funding Source: NIH RePORTER
- NCI NIH HHS [P50 CA097190, R01 CA098372] Funding Source: Medline
EGFR and its respective ligands are overexpressed in various tumors and this over-expression correlates with poor prognosis in selected cancers. In addition to direct activation by EGFR autocrine ligands, the large family of G-protein-coupled receptors (GPCRs) has been reported to transactivate EGFR via both ligand-dependent and independent mechanisms. GPCRs can induce the cleavage of membrane-bound EGFR-ligand precursors or directly activate the juxtamembrane tyrosine kinase domain of EGFR. Due to the heterogenous expression of GPCRs in tumors, this form of receptor crosstalk may contribute to the modest clinical responses to EGFR-targeted therapies observed to date. Studies, so far, have indicated that the signaling mechanisms involved in transactivation are specifically influenced by the activated GPCR and the tumor type in question. The progression of colon, lung, breast, head and neck, prostate and ovarian cancers have all been reported to be mediated, at least in part, by GPCR-EGFR crosstalk. Increased understanding of the specific signaling pathways involved in EGFR transactivation by GPCR will facilitate the identification of new biomarkers for molecular targeting strategies.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据