Disrupting the Scaffold to Improve Focal Adhesion Kinase-Targeted Cancer Therapeutics

被引：84

作者：

Cance, William G. ^{[1
,2
,3
]}

Kurenova, Elena ^{[1
,3
]}

Marlowe, Timothy ^{[1
]}

Golubovskaya, Vita ^{[1
,3
]}

机构：

[1] Roswell Pk Canc Inst, Buffalo, NY 14263 USA

[2] SUNY Buffalo, Dept Surg, Buffalo, NY 14263 USA

[3] CureFAKtor Pharmaceut LLC, Orchard Pk, NY 14127 USA

来源：

SCIENCE SIGNALING | 2013年 / 6卷 / 268期

关键词：

PROTEIN-TYROSINE KINASE; GROWTH-FACTOR RECEPTOR-3; CELL-MIGRATION; OVEREXPRESSION; APOPTOSIS; FAK; PHOSPHORYLATION; INHIBITOR; AUTOPHOSPHORYLATION; ASSOCIATION;

D O I：

10.1126/scisignal.2004021

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Focal adhesion kinase (FAK) is emerging as a promising cancer target because it is highly expressed at both the transcriptional and translational level in cancer and is involved in many aspects of tumor growth, invasion, and metastasis. Existing FAK-based therapeutics focus on inhibiting the kinase's catalytic function and not the large scaffold it creates that includes many oncogenic receptor tyrosine kinases and tumor suppressor proteins. Targeting the FAK scaffold is a feasible and promising approach for developing highly specific therapeutics that disrupt FAK signaling pathways in cancer.

引用

页数：3

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