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Cited by 537

The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.

Upregulation of CXCR4 is essential for HER2-mediated tumor metastasis

Open access
Li, Yan M., Pan, Yong, Wei, Yongkun, Cheng, Xiaoyun, Zhou, Binhua P., Tan, Ming, Zhou, Xiaoyan, Xia, Weiya, Hortobagyi, Gabriel N., Yu, Dihua, Hung, Mien-Chie·2004·Cancer Cell

Abstract

The receptor tyrosine kinase HER2 enhances tumor metastasis; however, its role in homing to metastatic organs is poorly understood. The chemokine receptor CXCR4 has recently been shown to mediate the movement of malignant cancer cells to specific organs. Here, we show that HER2 enhances the expression of CXCR4, which is required for HER2-mediated invasion in vitro and lung metastasis in vivo. HER2 also inhibits ligand-induced CXCR4 degradation. Finally, a significant correlation between HER2 and CXCR4 expression was observed in human breast tumor tissues, and CXCR4 expression correlated with a poor overall survival rate in patients with breast cancer. These results provide a plausible mechanism for HER2-mediated breast tumor metastasis and establish a functional link between HER2 and CXCR4 signaling pathways.

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Crossref · 10.1016/j.ccr.2004.09.027

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Metadata

Authors
Li, Y. M., Pan, Y., Wei, Y., Cheng, X., Zhou, B. P., Tan, M., Zhou, X., Xia, W., Hortobagyi, G. N., Yu, D., & Hung, M.-C.
Venue
Cancer Cell
Publisher
Elsevier BV
Published
2004-11
Volume
6
Issue
5
Pages
459-469
ISSN
1535-6108 (ISSN-L)
OpenAlex
W2018939316
Cited by
537
References
47
FWCI
13.66
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Upregulation of CXCR4 is essential for HER2-mediated tumor metastasis. https://app.cochat.ai/papers/10.1016/j.ccr.2004.09.027
The paper
Li, Y. M., Pan, Y., Wei, Y., Cheng, X., Zhou, B. P., Tan, M., Zhou, X., Xia, W., Hortobagyi, G. N., Yu, D., & Hung, M.-C. (2004). Upregulation of CXCR4 is essential for HER2-mediated tumor metastasis. Cancer Cell. https://doi.org/10.1016/j.ccr.2004.09.027

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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