Protein tyrosine phosphatases as novel targets in breast cancer therapy

被引：57

作者：

Nunes-Xavier, Caroline E. ^{[1
]}

Martin-Perez, Jorge ^{[2
]}

Elson, Ari ^{[3
]}

Pulido, Rafael ^{[1
,4
]}

机构：

[1] Hosp Cruces, BioCruces Hlth Res Inst, Baracaldo 48903, Spain

[2] Inst Invest Biomed A Sols CSIC UAM, Dpto Biol Canc, Madrid 28029, Spain

[3] Weizmann Inst Sci, Dept Mol Genet, IL-76100 Rehovot, Israel

[4] Basque Fdn Sci, Ikerbasque, Bilbao 48011, Spain

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER | 2013年 / 1836卷 / 02期

关键词：

Protein tyrosine phosphatase; Protein tyrosine kinase; Cell signaling; Therapy resistance; Drug targeting; Breast cancer; GROWTH-FACTOR RECEPTOR; SRC FAMILY KINASES; GAMMA PTP-GAMMA; SUPPRESSOR GENE PTPN13/PTPL1; CANDIDATE TUMOR-SUPPRESSOR; CELL-MIGRATION; C-SRC; SIGNAL-TRANSDUCTION; IN-VITRO; MOLECULAR-MECHANISM;

D O I：

10.1016/j.bbcan.2013.06.001

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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. (C) 2013 Elsevier B.V. All rights reserved.

引用

页码：211 / 226

页数：16

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