Quaking as a novel target of miR-200b to regulate tumor cell cycle progression mediated angiogenesis and metastasis

Tina H Nguyen, S. Alahari
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Abstract

Tumor growth is mediated by several factors including metabolic function, intracellular signaling, evasion of apoptosis, tissue invasion and metastasis, and angiogenesis. Of these factors, angiogenesis is a crucial component due to its part in both delivering nutrients and providing a conduit for metastasis. Current anti-angiogenic therapies focus on tumor-derived VEGF signaling; however, these efforts are modest and prone to resistance by upregulation of other pro-angiogenic signaling (1,2). Due to incomplete knowledge of endothelial cell (EC) biology, other methods of impeding tumor angiogenesis are not available.
作为miR-200b调节肿瘤细胞周期进程介导的血管生成和转移的新靶点
肿瘤生长由多种因素介导,包括代谢功能、细胞内信号传导、细胞凋亡逃避、组织侵袭和转移以及血管生成。在这些因素中,血管生成是一个至关重要的组成部分,因为它既能输送营养,又能为转移提供管道。目前的抗血管生成疗法侧重于肿瘤衍生的VEGF信号传导;然而,这些努力是适度的,并且容易通过上调其他促血管生成信号而产生耐药性(1,2)。由于对内皮细胞(EC)生物学的不完全了解,目前还没有其他阻止肿瘤血管生成的方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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