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The HOXB7 protein renders breast cancer cells resistant to tamoxifen through activation of the EGFR pathway
Journal article   Open access   Peer reviewed

The HOXB7 protein renders breast cancer cells resistant to tamoxifen through activation of the EGFR pathway

Kideok Jin, Xiangjun Kong, Tariq Shah, Marie-France Penet, Flonne Wildes, Dennis C. Sgroi, Xiao-Jun Ma, Yi Huang, Anne Kallioniemi, Goran Landberg, …
Proceedings of the National Academy of Sciences - PNAS, Vol.109(8), pp.2736-2741
02/21/2012
DOI: 10.1073/pnas.1018859108
PMCID: PMC3286915
PMID: 21690342
url
https://doi.org/10.1073/pnas.1018859108View
Published (Version of record) Open Access

Abstract

Multiple factors including long-term treatment with tamoxifen are involved in the development of selective estrogen receptor (ER) modulator resistance in ER alpha-positive breast cancer. Many underlying molecular events that confer resistance are known but a unifying theme is yet to be revealed. In this report, we provide evidence that HOXB7 overexpression renders MCF-7 cells resistant to tamoxifen via cross-talk between receptor tyrosine kinases and ER alpha signaling. HOXB7 is an ER alpha-responsive gene. Extended treatment of MCF-7 cells with tamoxifen resulted in progressively increasing levels of HOXB7 expression, along with EGFR and EGFR ligands. Up-regulation of EGFR occurs through direct binding of HOXB7 to the EGFR promoter, enhancing transcriptional activity. Finally, higher expression levels of HOXB7 in the tumor significantly correlated with poorer disease-free survival in ER alpha-positive patients with breast cancer on adjuvant tamoxifen monotherapy. These studies suggest that HOXB7 acts as a key regulator, orchestrating a major group of target molecules in the oncogenic hierarchy. Functional antagonism of HOXB7 could circumvent tamoxifen resistance.
Multidisciplinary Sciences Science & Technology Science & Technology - Other Topics

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