期刊
CANCER RESEARCH
卷 65, 期 15, 页码 6493-6497出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-04-1303
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资金
- NCI NIH HHS [R01 CA081419-06, CA 16672, R01 CA081419] Funding Source: Medline
Experimental evidence suggests that CXCR4, a G(i) protein-coupled receptor for the ligand CXCL12/stromal cell-derived factor-lot (SDF-1 alpha), plays a role in breast cancer metastasis. Transactivation of HER2-neu by G protein-coupled receptor activation has been reported as a ligand-independent mechanism of activating tyrosine kinase receptors. We found that SDF-1 alpha transactivated HER2-neu in the breast cancer cell lines MDA-MB-361 and SKBR3, which express both CXCR4 and HER2-neu. AMD3100, a CXCR4 inhibitor, PKI 166, an epidermal growth factor receptor/HER2-neu tyrosine kinase inhibitor, and PP2, a Src kinase inhibitor, each blocked SM-1 alpha-induced HER2-neu phosphorylation. Blocking Src kinase, with PP2 or using a kinase-inactive Src construct, and inhibiting epidermal growth factor receptor/HER2-neu signaling with PKI 166 each inhibited SDF-1 alpha-stimulated cell migration. We report a novel mechanism of HER2-neu transactivation through SDF-1 alpha stimulation of CXCR4 that involves Src kinase activation.
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