Regulation of Apoptosis by the Transforming Gene Products of Adenovirus

White, Eileen; Rao, Lakshmi G.; Chiou, Shiun-Kwei; Tseng, Ching‐Chun; Sabbatini, Peter; Gonzalez, Michelle; Verwaerde, Philippe

doi:10.1007/978-1-4757-9217-1_4

Cited by 8 publications

(8 citation statements)

References 74 publications

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“…Cold Spring Harbor Laboratory Press on May 13, 2018 -Published by genesdev.cshlp.org Downloaded from Howes et al 1994;Morgenbesser et al 1994;Pan and Griep 1994;White et al 1994;White 1996). In this study, we have provided in vivo evidence correlating the onset of unscheduled oncogene-driven cell proliferation with apoptosis during the preneoplastic stages of neoplastic transformation.…”

Section: Genes and Developmentmentioning

confidence: 64%

“…In one example, transformed epithelial cells expressing adenovirus E 1A accumulate slowly as a result of concordant cell death, which can be ameliorated by the presence of the death-protecting E1B 19K protein or bcl-2 (White et al 1994;White 1996). Thus, complete transformation of a cell may require both increased proliferative capacity and protection from apoptosis.…”

mentioning

confidence: 99%

“…dence for an interrelationship between cell death and cell transformation came from cell-culture studies indicating that expression of certain growth-stimulatory oncogenes leads to a paradoxical consequence of cell proliferation and cell death under conditions that restrict growth (Evan et al 1992;White et al 1994;White 1996). In one example, transformed epithelial cells expressing adenovirus E 1A accumulate slowly as a result of concordant cell death, which can be ameliorated by the presence of the death-protecting E1B 19K protein or bcl-2 (White et al 1994;White 1996).…”

mentioning

confidence: 99%

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The rise and fall of apoptosis during multistage tumorigenesis: down-modulation contributes to tumor progression from angiogenic progenitors.

Naik

Karrim²,

Hanahan³

1996

Genes Dev.

183

138

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In a mouse model of multistage tumorigenesis of islet 13-cells, apoptosis was activated concomitant with T-antigen oncogene-induced cell proliferation, further increased in the angiogenic stage, and markedly reduced in solid tumors. Crosses to p53-null mice confirmed this stage-specific variation as a p53-independent apoptotic process. Several apoptosis regulators were expressed, of which bcl-x L was up-regulated in tumors. When overexpressed throughout the pathway, bcl-xL protected most oncogene-expressing cells from apoptosis, enhancing progression from angiogenic progenitor to tumor without affecting earlier transitions. Further, two classes of solid tumor are described, distinguished by size and apoptotic incidence, implicating apoptosis regulation in expansive tumor growth. Thus, down-modulation of apoptosis selectively contributes to late steps in a tumorigenesis pathway.

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Section: Genes and Developmentmentioning

confidence: 64%

mentioning

confidence: 99%

mentioning

confidence: 99%

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The rise and fall of apoptosis during multistage tumorigenesis: down-modulation contributes to tumor progression from angiogenic progenitors.

Naik

Karrim²,

Hanahan³

1996

Genes Dev.

183

138

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“…This is consistent with the finding of a reduced rate of cell death in the H-ras-expressing p53A derivatives. Furthermore, promoting cell proliferation frequently is associated with accelerated cell death (as E1A and E2F act) (38,42,44,51) and not maintenance of cell viability. In this setting, suppression of cell death may play a more important role than does enhancing cell replication in countering cell loss through apoptosis.…”

Section: Vol 15 1995 Activated H-ras Rescue Of E1a-induced Apoptosimentioning

confidence: 99%

“…E1A expression induces p53 accumulation (5,24), which mimics the cellular response to DNA damage upon UV or ionizing radiation treatments (19,21,28). Furthermore, dominant interfering mutant p53, cellular oncoprotein Mdm-2, and the E1B 55K protein, which directly bind to p53 and modulate p53 function (3,35,50), can cooperate with E1A to transform BRK cells (8,40,44), demonstrating that abrogation of wild-type p53 functions prevents cell death. Finally, E1A alone can transform p53-deficient (p53…”

mentioning

confidence: 99%

Activated H-ras Rescues E1A-Induced Apoptosis and Cooperates with E1A To Overcome p53-Dependent Growth Arrest

Lin

Eviner

Prendergast

et al. 1995

Molecular and Cellular Biology

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The adenovirus E1A oncogene products stimulate DNA synthesis and cell proliferation but fail to transform primary baby rat kidney (BRK) cells because of the induction of p53-mediated programmed cell death (apoptosis). Overexpression of dominant mutant p53 (to abrogate wild-type p53 function) or introduction of apoptosis inhibitors, such as adenovirus E1B 19K or Bcl-2 oncoproteins, prevents E1A-induced apoptosis and permits transformation of BRK cells. The ability of activated Harvey-ras (H-ras) to cooperate with E1A to transform BRK cells suggests that H-ras is capable of overcoming the E1A-induced, p53-dependent apoptosis. We demonstrate here that activated H-ras was capable of suppressing apoptosis induced by E1A and wild-type p53. However, unlike Bcl-2 and the E1B 19K proteins, which completely block apoptosis but not p53-dependent growth arrest, H-ras expression permitted DNA synthesis and cell proliferation in the presence of high levels of wild-type p53. The mechanism by which H-ras regulates apoptosis and cell cycle progression is thereby strikingly different from that of the E1B 19K and Bcl-2 proteins. BRK cells transformed with H-ras and the temperature sensitive murine mutant p53(val 135), which lack E1A, underwent growth arrest at the permissive temperature for wild-type p53. p53-dependent growth arrest, however, could be relieved by E1A expression. Thus, H-ras alone was insufficient and cooperation of H-ras and E1A was required to override growth suppression by p53. Our data further suggest that two complementary growth signals from E1A plus H-ras can rescue cell death and thus permit transformation.

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Regulation of Apoptosis by Adenovirus E1A and E1B Oncogenes

White

1998

Seminars in Virology

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Regulation of Apoptosis by the Transforming Gene Products of Adenovirus

Cited by 8 publications

References 74 publications

The rise and fall of apoptosis during multistage tumorigenesis: down-modulation contributes to tumor progression from angiogenic progenitors.

The rise and fall of apoptosis during multistage tumorigenesis: down-modulation contributes to tumor progression from angiogenic progenitors.

Activated H-ras Rescues E1A-Induced Apoptosis and Cooperates with E1A To Overcome p53-Dependent Growth Arrest

Regulation of Apoptosis by Adenovirus E1A and E1B Oncogenes

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