Bissonnette R P, Echeverri F, Mahboubi A, Green D R
Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, California 92037.
Nature. 1992 Oct 8;359(6395):552-4. doi: 10.1038/359552a0.
Apoptosis is a form of physiological cell death, characterized by chromatin condensation, cytoplasmic blebbing and DNA fragmentation, which often depends on RNA and protein synthesis by the dying cell. The c-myc proto-oncogene, usually implicated in cell transformation, differentiation and cell-cycle progression also has a central role in some forms of apoptosis. These opposing roles of myc in cell growth and death require that other gene products dictate the outcome of c-Myc expression on a cell. A candidate for such a modifying gene is bcl-2, whose product prolongs cell survival and blocks apoptosis in some systems. Here we demonstrate that Bcl-2 prevents apoptotic death induced by c-Myc, provide a mechanism whereby cells can express c-Myc without undergoing apoptosis, and give a possible explanation for the ability of Bcl-2 to synergize with c-Myc in cell transformation.
细胞凋亡是一种生理性细胞死亡形式,其特征为染色质浓缩、细胞质起泡和DNA片段化,这通常依赖于濒死细胞的RNA和蛋白质合成。c-myc原癌基因通常与细胞转化、分化和细胞周期进程有关,在某些形式的细胞凋亡中也起核心作用。myc在细胞生长和死亡中的这些相反作用要求其他基因产物决定c-Myc在细胞上表达的结果。这种修饰基因的一个候选者是bcl-2,其产物在某些系统中可延长细胞存活并阻止细胞凋亡。在此我们证明Bcl-2可防止由c-Myc诱导的凋亡性死亡,提供一种细胞能够表达c-Myc而不发生凋亡的机制,并对Bcl-2在细胞转化中与c-Myc协同作用的能力给出一种可能的解释。