DELETION OF A NONCONSERVED REGION OF BCL-2 CONFERS A NOVEL GAIN OF FUNCTION - SUPPRESSION OF APOPTOSIS WITH CONCOMITANT CELL-PROLIFERATION

The Bcl-2 protein coded by the proto-oncogene bcl-2 is expressed in a variety of embryonic and postnatal tissues and is overproduced in seve ral types of tumors. Bcl-2 expression suppresses apoptosis induced by a multitude of stimuli in diverse cell types without exerting signific ant effects on cell proliferation, and is believed to contribute to on cogenesis by extending cell survival, In certain B-cell lymphomas, chr omosomal translocations result in a gain of function of Bcl-2 by overe xpression, Here, we report that a deletion of a nonconserved region of human Bcl-2 (residues 51-85) confers a novel gain of function that no t only suppresses apoptosis induced by the tumor suppressor protein p5 3 and the Myc oncoprotein but also permits continued cell proliferatio n, Our result raises the possibility that mutations within the bcl-2 g ene may contribute to oncogenesis by both suppressing apoptosis and fa cilitating cell proliferation.