Ha-ras Oncogene and Anticancer Drug Resistance

Giri Raghavaraju , Hsiao-Sheng Liu
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引用次数: 3

Abstract

Extensive research on the Ras proteins and their functions in cell physiology over the past 30 years has led to copious approaches that reported the possible role of Ras not only in tumorigenesis but also in many developmental disorders. One of the hallmarks of human cancers is the intrinsic resistance to apoptosis. In this review we focus on anticancer drug sensitivities towards Ha-ras oncogene overexpression in vitro, reveal the downstream Ras effector molecules involved in the signaling pathways and the effect on cell cycle progression. Furthermore, we particularly emphasized 5-fluorouracil, Lovastatin, Tumor necrosis factor-α and Xanthone in selective suppression of Ha-ras-related tumorigenesis. Hence, a better understanding of the molecular mechanisms underlying tumor sensitivity to apoptotic cell death is anticipated to provide the basis for a rational approach to develop molecular targeted therapies.

Ha-ras癌基因与抗癌耐药
在过去的30年里,对Ras蛋白及其在细胞生理学中的功能的广泛研究导致了大量的方法报道Ras不仅在肿瘤发生中可能起作用,而且在许多发育障碍中也可能起作用。人类癌症的特征之一是对细胞凋亡的内在抵抗。本文综述了抗肿瘤药物在体外对Ha-ras癌基因过表达的敏感性,揭示了下游Ras效应分子参与的信号通路及其对细胞周期进程的影响。此外,我们特别强调5-氟尿嘧啶、洛伐他汀、肿瘤坏死因子-α和山酮在选择性抑制ha -ras相关肿瘤发生中的作用。因此,更好地了解肿瘤对凋亡细胞死亡敏感性的分子机制有望为开发分子靶向治疗的合理方法提供基础。
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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