Upregulation of CXCR4 is essential for HER2-mediated tumor metastasis
Yan Michael Li,Yong Pan,Yongkun Wei,Xiaoyun Cheng,Xiaoyun Cheng,Binhua P. Zhou,Ming Tan,Xiaoyan Zhou,Weiya Xia,Gabriel N. Hortobagyi,Dihua Yu,Dihua Yu,Mien Chie Hung,Mien Chie Hung +13 more
TLDR
It is shown that HER2 enhances the expression of CXCR4, which is required for HER2-mediated invasion in vitro and lung metastasis in vivo, and this work establishes a functional link between HER2 and CX CR4 signaling pathways.About:
This article is published in Cancer Cell.The article was published on 2004-11-01 and is currently open access. It has received 515 citations till now. The article focuses on the topics: Metastasis & Receptor tyrosine kinase.read more
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Microenvironmental regulation of metastasis
TL;DR: Experimental data demonstrating the role of the microenvironment in metastasis is described, areas for future research are identified and possible new therapeutic avenues are suggested.
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G-protein-coupled receptors and cancer.
TL;DR: This Review will address the current understanding of the many roles of GPCRs and their signalling circuitry in tumour progression and metastasis and discuss how interfering with GPCR might provide unique opportunities for cancer prevention and treatment.
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CXCR4: a key receptor in the crosstalk between tumor cells and their microenvironment.
TL;DR: Observations reveal that CXCR4 is an important molecule involved in the spread and progression of a variety of different tumors, and that CxCR4 antagonists, although initially developed for treatment of AIDS, actually may become effective agents for the treatment of neoplastic disease.
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Detection, clinical relevance and specific biological properties of disseminating tumour cells
TL;DR: The evidence that disseminating tumour cells have a variety of uses for understanding tumour biology and improving cancer treatment is reviewed.
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The oncogene HER2; Its signaling and transforming functions and its role in human cancer pathogenesis
TL;DR: An abundance of experimental evidence now solidly supports the HER2 oncogene hypothesis and etiologically links amplification of the HER1 gene locus with human cancer pathogenesis and suggests that HER2 may indeed induce cell transformation through multiple mechanisms.
References
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