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Invadopodia: At the cutting edge of tumour invasion.

机译:Invadopodia:在肿瘤侵袭的最前沿。

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摘要

Invasion of tissues by malignant tumours is facilitated by tumour cell migration and degradation of extracellular matrix (ECM) barriers. Several invasive neoplasms, including head and neck squamous cell carcinoma, breast carcinoma, melanoma and glioma, contain tumour cells that can form actin-rich protrusions with ECM proteolytic activity called invadopodia. These dynamic organelle-like structures adhere to, and digest, collagens, laminins and fibronectin. Invadopodia are dependent on multiple transmembrane, cytoplasmic and secreted proteins engaged in cell adhesion, signal transduction, actin assembly, membrane regulation and ECM proteolysis. Strategies aimed at disrupting invadopodia could form the basis of novel anti-invasive therapies for treating patients. Here we review the molecular basis of invadopodia formation with particular emphasis on the intracellular signaling networks that are essential for invadopodia activity and examine the potential role of these structures in glioma invasion.
机译:肿瘤细胞迁移和细胞外基质(ECM)屏障的降解促进了恶性肿瘤对组织的侵袭。包括头颈部鳞状细胞癌,乳腺癌,黑色素瘤和神经胶质瘤在内的几种侵袭性肿瘤所含的肿瘤细胞可以形成富含肌动蛋白的突起,具有ECM蛋白水解活性,称为invadopodia。这些动态的细胞器样结构粘附并消化胶原蛋白,层粘连蛋白和纤连蛋白。 Invadopodia依赖于参与细胞粘附,信号转导,肌动蛋白组装,膜调节和ECM蛋白水解的多个跨膜,胞质和分泌蛋白。旨在破坏侵袭性足病的策略可构成治疗患者的新型抗侵入疗法的基础。在这里,我们审查了昆虫足形成的分子基础,特别是对于昆虫足活动必不可少的细胞内信号网络,并研究了这些结构在神经胶质瘤侵袭中的潜在作用。

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