癌症中的细胞凋亡:从发病机制到晚期选择性Bcl-2家族抑制剂的发现

Samaa Abbas, N. Abdou, Deena S. Lasheen, D. Ella
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引用次数: 3

摘要

癌症是一种遗传疾病,具有两个特征:细胞生长不受调节和组织侵袭(转移)。它可以看作是一系列遗传变化的结果,在此期间,正常细胞转变为恶性细胞。逃避细胞死亡,细胞凋亡,是细胞中导致这种恶性转化的基本变化之一。因此,细胞凋亡的减少或其抵抗在癌变中起着至关重要的作用。Bcl-2家族蛋白调控线粒体凋亡途径。疾病状态出现在Bcl-2蛋白家族失调时,细胞死亡要么被促进,要么被逃避;抗凋亡蛋白的过度表达是癌细胞促进生存最常用的策略之一。具体而言,Bcl-2过表达已被证明是许多人类癌症的主要化疗耐药因素,因此,Bcl-2靶向是寻求重新激活细胞死亡以获得癌症治疗益处的药理学重点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Apoptosis in cancer: from pathogenesis to discovery of advanced selective Bcl-2 family inhibitors
Cancer is a genetic disease characterized by two features: unregulated cell growth and tissue invasion (metastasis). It can be viewed as the result of a succession of genetic changes during which a normal cell is transformed into a malignant one. Evasion of cell death, apoptosis, is one of the essential changes in a cell that cause this malignant transformation. Hence, reduced apoptosis or its resistance plays a vital role in carcinogenesis. The Bcl-2 family of proteins regulates the mitochondrial apoptotic pathway. Disease states arise upon deregulation of the Bcl-2 family of proteins, where cell death is either promoted or evaded; one of the most common tactic cancer cells utilize to promote survival is anti-apoptotic protein overexpression. Specifically, Bcl-2 overexpression has been shown to be a major chemoresistance factor in a number of human cancers, and for this reason, Bcl-2 targeting is a pharmacologic priority in the quest to reactivate cell death for therapeutic benefit in cancer.
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