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SHP2 is a multifunctional therapeutic target in drug resistant metastatic breast cancer
Journal article   Open access   Peer reviewed

SHP2 is a multifunctional therapeutic target in drug resistant metastatic breast cancer

Hao Chen, Sarah Libring, Kasi Viswanatharaju Ruddraraju, Jinmin Miao, Luis Solorio, Zhong-Yin Zhang and Michael K. Wendt
Oncogene, Vol.39(49), pp.7166-7180
12/03/2020
DOI: 10.1038/s41388-020-01488-5
PMCID: 7714690
PMID: 33033382
url
https://doi.org/10.1038/s41388-020-01488-5View
Published (Version of record) Open Access

Abstract

Metastatic breast cancer (MBC) is an extremely recalcitrant disease capable of bypassing current targeted therapies via engagement of several growth promoting pathways. SH2 containing protein tyrosine phosphatase-2 (SHP2) is an oncogenic phosphatase known to facilitate growth and survival signaling downstream of numerous receptor inputs. Herein, we used inducible genetic depletion and two distinct pharmacological inhibitors to investigate the therapeutic potential of targeting SHP2 in MBC. Cells that acquired resistance to the ErbB kinase inhibitor, neratinib, displayed increased phosphorylation of SHP2 at the Y542 activation site. In addition, higher levels of SHP2 phosphorylation, but not expression, were associated with decreased survival of breast cancer patients. Pharmacological inhibition of SHP2 activity blocked ERK1/2 and AKT signaling generated from exogenous stimulation with FGF2, PDGF, and hGF and readily prevented MBC cell growth induced by these factors. SHP2 was also phosphorylated upon engagement of the extracellular matrix (ECM) via focal adhesion kinase. Consistent with the potential of SHP2-targeted compounds as therapeutic agents, the growth inhibitory property of SHP2 blockade was enhanced in ECM-rich 3D culture environments. In vivo blockade of SHP2 in the adjuvant setting decreased pulmonary metastasis and extended the survival of systemic tumor-bearing mice. Finally, inhibition of SHP2 in combination with FGFR-targeted kinase inhibitors synergistically blocked the growth of MBC cells. Overall, our findings support the conclusion that SHP2 constitutes a shared signaling node allowing MBC cells to simultaneously engage a diversity of growth and survival pathways, including those derived from the ECM.
Cell Biology Oncology Biochemistry & Molecular Biology Genetics & Heredity Life Sciences & Biomedicine Science & Technology

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