Cytoskeletal network in colon cancer: from genes to clinical application
Cytoskeletal network in colon cancer: from genes to clinical application
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DOI：
10.1016/j.biocel.2003.09.004
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发表时间：
2004-05-01
影响因子：
4
通讯作者：
Pignatelli, M
中科院分区：
文献类型：
--
作者：
Buda, A;Pignatelli, M
结直肠癌是由明确的连续步骤引起的，其特征是不同的遗传事件。细胞粘附分子的表达和功能活性的异常与大多数结直肠癌的发生和进展有关。细胞间（例如E-钙粘蛋白/连环蛋白复合物）和细胞基质（例如整合素）粘附分子不仅仅是胶结物质，还调节细胞极性、分化、增殖、迁移和侵袭。许多这些细胞事件是通过它们与肌动蛋白细胞骨架网络的密切联系来介导的。动态肌动蛋白细胞骨架是正常上皮细胞的特征，肌动蛋白丝的聚合和解聚使细胞形状在迁移和有丝分裂过程中发生变化。在结直肠癌中，当细胞变得具有侵袭性时，它们会失去肌动蛋白细胞骨架组织和正常的细胞粘附力。未来的研究应该能够揭示肿瘤生物学中新的细胞骨架网络功能，并可能导致基于操纵其相关分子的新治疗策略的开发。 (C) 2003 Elsevier Ltd. 保留所有权利。
Colorectal cancer arises from well-defined sequential steps characterised by distinct genetic events. Abnormalities in the expression and functional activity of cell adhesion molecules are implicated in the development and progression of the majority of colorectal cancers. Intercellular (e.g. E-cadherin/catenin complex) and cell-matrix (e.g. integrins) adhesion molecules are more than just cementing substances but regulate cell polarity, differentiation, proliferation, migration and invasion. Many of these cellular events are mediated through their intimate association with the actin cytoskeletal network. A dynamic actin cytoskeleton characterises normal epithelial cells and polymerisation and depolymerisation of actin filaments enables cell shape to change during migration and mitosis. In colorectal cancer, cells lose actin cytoskeletal organisation and normal cell adhesion when they become invasive. Future investigations should allow the unravelling of new cytoskeletal network functions in tumour biology and may lead to the development of novel therapeutic strategies based on the manipulation of its associated molecules. (C) 2003 Elsevier Ltd. All rights reserved.