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首页> 外文期刊>Pharmaceutical research >Inhibition of tumor angiogenesis by tumstatin: insights into signaling mechanisms and implications in cancer regression.
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Inhibition of tumor angiogenesis by tumstatin: insights into signaling mechanisms and implications in cancer regression.

机译：肿瘤抑素抑制肿瘤血管生成：深入了解信号传导机制及其对癌症消退的影响。

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摘要

Growing tumors develop additional new blood vessels to meet the demand for adequate nutrients and oxygen, a process called angiogenesis. Cancer is a highly complex disease promoted by excess angiogenesis; interfering with this process poses for an attractive approach for controlling tumor growth. This hypothesis led to the identification of endogenous angiogenesis inhibitors generated from type IV collagen, a major component of vascular basement membrane (VBM). Type IV collagen and the angiogenesis inhibitors derived from it are involved in complex roles, than just the molecular construction of basement membranes. Protease degradation of collagens in VBM occurs in various physiological and pathological conditions and produces several peptides. Some of these peptides are occupied in the regulation of functions conflicting from those of their original integral molecules. Tumstatin (alpha3(IV)NC1), a proteolytic C-terminal non-collagenous (NC1) domain from type IV collagen alpha3 chain has been highlighted recently because of its potential role in anti-angiogenesis, however its biological actions are not limited to these processes. alpha3(IV)NC1 inhibits proliferation by promoting endothelial cell apoptosis and suppresses diverse tumor angiogenesis, thus making it a potential candidate for future cancer therapy. The present review surveys the physiological functions of type IV collagen and discovery of alpha3(IV)NC1 as an antiangiogenic protein with a comprehensive overview of the knowledge gained by us towards understanding its signaling mechanisms.
机译：生长中的肿瘤会发展出新的新血管，以满足对充足营养和氧气的需求，这一过程称为血管生成。癌症是由过度血管生成促进的高度复杂的疾病。干扰该过程为控制肿瘤生长提供了一种有吸引力的方法。该假设导致鉴定了由IV型胶原蛋白（血管基底膜（VBM）的主要成分）产生的内源性血管生成抑制剂。 IV型胶原蛋白及其衍生的血管生成抑制剂不仅具有基底膜的分子结构，而且还具有复杂的作用。 VBM中胶原蛋白的蛋白酶降解发生在各种生理和病理条件下，并产生几种肽。这些肽中的一些占据了与其原始整体分子的功能相反的功能的调节。 Tumstatin（alpha3（IV）NC1），来自IV型胶原蛋白alpha3链的蛋白水解C端非胶原（NC1）域，由于其在抗血管生成中的潜在作用而最近被重点研究，但是其生物学作用不限于这些流程。 alpha3（IV）NC1通过促进内皮细胞凋亡抑制增殖，并抑制多种肿瘤血管生成，因此使其成为未来癌症治疗的潜在候选者。本综述综述了IV型胶原的生理功能以及作为抗血管生成蛋白的alpha3（IV）NC1的发现，并全面概述了我们了解其信号传导机制所获得的知识。

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