Induction of ornithine decarboxylase by IL-3 is mediated by sequential c-Myc-independent and c-Myc-dependent pathways

Packham, Graham; Cleveland, John L.

doi:10.1038/sj.onc.1201273

Cited by 43 publications

(50 citation statements)

References 42 publications

(97 reference statements)

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“…Although it was initially thought that cMyc induced apoptosis was p53-dependent, subsequent study demonstrated the occurrence of c-Myc induced apoptosis in ®broblasts transfected with SV40 T antigen to ablate p53 function (Lenehan and Ozer, 1996). It is not certain which c-Myc target genes are required for induction of apoptosis, but recent studies have identi®ed two possible candidates: ornithine decarboxylase and the CDC25A cell cycle phosphatase (Packham et al, 1996;Galaktonor et al, 1996). We found that while SF and ADR by themselves each caused an increase in c-Myc protein expression, pretreatment with SF blocked the ADR-induced increase in c-Myc protein levels.…”

Section: Discussionmentioning

confidence: 66%

“…Another major mechanism of induction of apoptosis is the enforced expression of c-Myc in growth factordeprived cells (Packham et al, 1996;Lenehan and Ozer, 1996). Although it was initially thought that cMyc induced apoptosis was p53-dependent, subsequent study demonstrated the occurrence of c-Myc induced apoptosis in ®broblasts transfected with SV40 T antigen to ablate p53 function (Lenehan and Ozer, 1996).…”

Section: Discussionmentioning

confidence: 99%

“…Over-expression of c-Myc in growth factor-deprived cells can induce apoptosis, both by p53-dependent and p53-independent mechanisms (Packham et al, 1996;Lenahan and Ozer, 1996). We examined the protein levels of various members of the c-Myc transcriptional network (HuÈ rlin et al, 1993(HuÈ rlin et al, , 1994 in MDA-MB-453 cells (see Figure 5b).…”

Section: Sf Protection Requires a Functional C-met Receptormentioning

confidence: 99%

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Scatter factor protects epithelial and carcinoma cells against apoptosis induced by DNA-damaging agents

et al. 1998

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Section: Discussionmentioning

confidence: 66%

Section: Discussionmentioning

confidence: 99%

Section: Sf Protection Requires a Functional C-met Receptormentioning

confidence: 99%

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Scatter factor protects epithelial and carcinoma cells against apoptosis induced by DNA-damaging agents

et al. 1998

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“…This dominant negative version of Myc has been used extensively in other systems to functionally block the oncogene. (21,51,52) In-32 and In-36 cells were unable to form OCLs and they showed a significant reduction in the expression of TRAP and cathepsin K, indicating a delay in the differentiation process.…”

Section: C-myc Role In Osteoclastogenesismentioning

confidence: 99%

c-myc Is Required for Osteoclast Differentiation

Battaglino¹,

D²,

Fu³

et al. 2002

Journal of Bone and Mineral Research

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The role of the receptor activator of nuclear factor B (NF-B) ligand (RANKL)-a tumor necrosis factor (TNF)-related cytokine-in osteoclast formation has been established clearly. However, the downstream signaling pathways activated by this cytokine remain largely unknown. To identify genes that play a role in osteoclastogenesis, we used RAW 264.7 mouse monocytes as a model system for the differentiation of multinucleated osteoclasts from mononucleated precursors. RAW 264.7 cells were induced with RANKL to form multinucleated giant osteoclast-like cells (OCLs) that expressed a number of osteoclast-specific markers and were able to form resorption pits on both calcium phosphate films and bone slices. This system was used to identify genes that are regulated by RANKL and may play a role in osteoclast differentiation.

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“…It has been reported recently that high levels of ornithine decarboxylase (ODC), a transcriptional target of Myc, can induce apoptosis, which is not accompanied by dysregulation of cell cycle control. Nonetheless, ODC was required downstream of Myc for myeloid cell growth, suggesting that c-Myc-induced pathways leading to cell cycle progression and apoptosis are separable, yet they share common mediators (Packham et al, 1996). For E2F-1 it has been shown, that its apoptotic function is separable from the ability to accelerate entry into DNA synthesis.…”

mentioning

confidence: 99%

Different regulation of c-Myc- and E2F-1-induced apoptosis during the ongoing cell cycle

Hengstschläger

Hölzl

Hengstschläger-Ottnad

1999

Oncogene

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The transcription factors c-Myc and E2F-1 have been shown to harbour both mitogenic and apoptotic properties. Both factors have been implicated in the regulation of the transition from the G1 phase to the S phase in the mammalian cell cycle. However, whether cell death triggered by these molecules is dependent on the cell's position in the ongoing cell cycle remained elusive. Using centrifugal elutriation we here show for the ®rst time that c-Myc induces apoptosis in G1 and in G2 phase, whereas E2F-1-induced apoptosis speci®cally occurs in G1. S phase cells are resistant to cell death triggered by these factors. We demonstrate that this is not a general phenomenon, since S phase cells are susceptible to apoptosis induced by treatment with actinomycin D and to the anti-apoptotic activity of Bcl-2. Our data indicate that S phase cells harbour speci®c protective activities against c-Myc-and E2F-1-induced apoptosis. Our results demonstrate that these transcription factors, although probably sharing speci®c apoptotic pathways, also take distinct routes to induce cell death and that apoptosis can occur at di erent phases of the cell cycle depending on the apoptotic stimulus. In this report we present the usefulness of a new approach to determine the regulation of apoptosis in the ongoing unperturbated cell cycle. This approach has clear implications for the identi®cation of target genes involved in the regulation of cell death.

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Induction of ornithine decarboxylase by IL-3 is mediated by sequential c-Myc-independent and c-Myc-dependent pathways

Cited by 43 publications

References 42 publications

Scatter factor protects epithelial and carcinoma cells against apoptosis induced by DNA-damaging agents

Scatter factor protects epithelial and carcinoma cells against apoptosis induced by DNA-damaging agents

c-myc Is Required for Osteoclast Differentiation

Different regulation of c-Myc- and E2F-1-induced apoptosis during the ongoing cell cycle

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