Breast cancer is linked to hyperactivation of protein tyrosine kinases (PTKs), and recent studies have unveiled that selective tyrosine dephosphorylation by protein tyrosine phosphatases (PTPs) of specific substrates, including PTKs, may activate or inactivate oncogenic pathways in human breast cancer cell growth-related processes. Here, we review the current knowledge on the involvement of PTPs in breast cancer, as major regulators of breast cancer therapy-targeted PTKs, such as HER1/EGFR, HER2/Neu, and Src. The functional interplay between PTKs and PTK-activating or -inactivating PTPs, and its implications in novel breast cancer therapies based on targeting of specific PTPs, are discussed.
Keywords: 17β-estradiol; Asp; BC; BCCL; Breast cancer; CNS; Cell signaling; Cys; DUSP; Drug targeting; E2; EGFR; ER; ERK; HER; HGR; IGF1R; IR; JAK; JMML; JNK; Janus kinase; LS; MAPK; NS; PDGFR; PR; PTK; PTP; PTPN/NRPTP; PTPR/RPTP; Protein tyrosine kinase; Protein tyrosine phosphatase; SFK; SNP; STAT; Ser; Signal transducer and activator of transcription; Src-family kinase; TNBC; Therapy resistance; Thr; Tyr; VEGFR; aspartic acid; breast cancer; breast cancer cell line; c-Jun N-terminal kinase; central nervous system; cysteine; dual specificity phosphatase; epidermal growth factor receptor; estrogen receptor; extracellular-signal regulated kinase; hormone growth receptor; human epidermal growth factor receptor; insulin growth factor-like 1 receptor; insulin receptor; juvenile myeolomonocytic leukaemia; leopard syndrome; mAb; mTOR; mammalian target of rapamycin; mitogen-activated protein kinase; monoclonal antibody; non-receptor PTP; noonan syndrome; platelet-derived growth factor receptor; progesterone receptor; protein tyrosine kinase; protein tyrosine phosphatase; receptor-like PTP; serine; single-nucleotide polymorphism; threonine; triple negative breast cancer; tyrosine; vascular–endothelial growth factor receptor.
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