Nunes-Xavier Caroline E, Martín-Pérez Jorge, Elson Ari, Pulido Rafael
BioCruces Health Research Institute, Hospital de Cruces, Plaza Cruces s/n, 48903 Barakaldo, Spain.
Biochim Biophys Acta. 2013 Dec;1836(2):211-26. doi: 10.1016/j.bbcan.2013.06.001. Epub 2013 Jun 10.
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.
乳腺癌与蛋白酪氨酸激酶（PTK）的过度激活有关，最近的研究表明，蛋白酪氨酸磷酸酶（PTP）对包括PTK在内的特定底物进行选择性酪氨酸去磷酸化，可能会激活或失活人类乳腺癌细胞生长相关过程中的致癌途径。在此，我们综述了关于PTP作为乳腺癌治疗靶点PTK（如HER1/EGFR、HER2/Neu和Src）的主要调节因子在乳腺癌中作用的现有知识。我们还讨论了PTK与激活或失活PTK的PTP之间的功能相互作用，以及其在基于靶向特定PTP的新型乳腺癌治疗中的意义。
