New approaches to targeting the actin cytoskeleton for chemotherapy

被引:37
作者
Bonello, Teresa T. [1 ]
Stehn, Justine R. [1 ]
Gunning, Peter W. [1 ]
机构
[1] Univ New S Wales, Sch Med Sci, Oncol Res Unit, Sydney, NSW 2052, Australia
基金
英国医学研究理事会;
关键词
ALDRICH-SYNDROME PROTEIN; MYOSIN II-B; EXTRACELLULAR-MATRIX DEGRADATION; SMALL-MOLECULE INHIBITORS; SQUAMOUS-CELL CARCINOMA; GROWTH-FACTOR RECEPTOR; BREAST-CANCER CELLS; INVASION IN-VITRO; ARP2/3; COMPLEX; N-WASP;
D O I
10.4155/FMC.09.99
中图分类号
R914 [药物化学];
学科分类号
100705 [微生物与生化药学];
摘要
The actin cytoskeleton is indispensable for normal cellular function. In particular, several actin-based structures coordinate cellular motility, a process hijacked by tumor cells in order to facilitate their propagation to distant sites. The actin cytoskeleton, therefore, represents a point for chemotherapeutic intervention. The challenge in disrupting the actin cytoskeleton is in preserving actin-driven contraction of cardiac and skeletal muscle. By targeting actin-binding proteins with altered expression in malignancy, it may be possible to achieve tumor-specific toxicity. A number of actin-binding proteins act cooperatively and synergistically to regulate actin structures required for motility. The actin cytoskeleton is characterized by a significant degree of plasticity. Targeting specific actin-binding proteins for chemotherapy will only be successful if no other compensatory mechanisms exist.
引用
收藏
页码:1311 / 1331
页数:21
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