Prevention of programmed cell death in burkitt lymphoma cell lines by bcl‐2‐dependent and ‐independent mechanisms
摘要：
Burkitt lymphoma (BL) cell lines which retain the phenotypic characteristics of the freshly-isolated tumour cells (group I cells) readily enter programmed cell death (apoptosis) in response to a variety of triggers. By contrast, isogenic BL cells which are phenotypically altered as a result of activation of their resident EBV genome (group-III cells) are highly protected from apoptosis. Phenotypic changes in group-III cells include the up-regulation of the oncogene, bcl -2. Expression of the 26-kDa bcl -2 protein in group-1 BL cells following gene transfer was found to afford protection from apoptosis: the degree of protection was proportional to the amount of bcl -2 protein expressed. When group-1 bcl -2 transfectants were compared with their group-III counterparts it was found that, whilst bcl -2 made a significant contribution in protecting from entry into apoptosis, hyper-expression of bcl -2 protein in group-1 cells (well beyond that of group-III cells) was necessary to attain the high levels of protection observed in group-III cells. These results suggested that additional, bcl -2-independent, survival mechanisms could operate in BL cells. In support of this notion it was also found that: (I) prolonged culture of group-1 lines in vitro resulted in enhanced survival in the absence of bcl -2 up-regulation, and (2) exposure of group-1 cells to interferon- triggered a bcl -2-independent protective response. The molecular mechanisms of both the bcl -2-dependent and -independent survival pathways remain to be determined. © 1992 Wiley-Liss, Inc.
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DOI：
10.1002/ijc.2910520424
被引量：
年份：
1992
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