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c-Myc and Her2 cooperate to drive a stem-like phenotype with poor prognosis in breast cancer
Journal article   Peer reviewed

c-Myc and Her2 cooperate to drive a stem-like phenotype with poor prognosis in breast cancer

R. Nair, D.L. Roden, W.S. Teo, A. McFarland, S. Junankar, S. Ye, A. Nguyen, J. Yang, I. Nikolic, M. Hui, …
Oncogenesis, Vol.33(30), pp.3992-4002
2014
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Abstract

The HER2 (ERBB2) and MYC genes are commonly amplified in breast cancer, yet little is known about their molecular and clinical interaction. Using a novel chimeric mammary transgenic approach and in vitro models, we demonstrate markedly increased self-renewal and tumour-propagating capability of cells transformed with Her2 and c-Myc. Coexpression of both oncoproteins in cultured cells led to the activation of a c-Myc transcriptional signature and acquisition of a self-renewing phenotype independent of an epithelial–mesenchymal transition programme or regulation of conventional cancer stem cell markers. Instead, Her2 and c-Myc cooperated to induce the expression of lipoprotein lipase, which was required for proliferation and self-renewal in vitro. HER2 and MYC were frequently coamplified in breast cancer, associated with aggressive clinical behaviour and poor outcome. Lastly, we show that in HER2+ breast cancer patients receiving adjuvant chemotherapy (but not targeted anti-Her2 therapy), MYC amplification is associated with a poor outcome. These findings demonstrate the importance of molecular and cellular context in oncogenic transformation and acquisition of a malignant stem-like phenotype and have diagnostic and therapeutic consequences for the clinical management of HER2+ breast cancer.

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Collaboration types
Domestic collaboration
International collaboration
Citation topics
1 Clinical & Life Sciences
1.108 Molecular & Cell Biology - Cancer & Development
1.108.591 Cancer Stem Cells
Web Of Science research areas
Biochemistry & Molecular Biology
Cell Biology
Genetics & Heredity
Oncology
ESI research areas
Molecular Biology & Genetics
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