Increased rate of degradation of c-myc mRNA in interferon-treated Daudi cells.

Dani, Christian; Mechti, Nadir; Piechaczyk, Marc; Lebleu, Bernard; Jeanteur, P; Blanchard, Jean Marie

doi:10.1073/pnas.82.15.4896

Cited by 179 publications

(79 citation statements)

References 35 publications

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“…11 As a follow-up study, Dani et al demonstrated in Daudi cells that IFN a/b did not affect the transcription rate of c-myc mRNA, but rather reduced the half-life of this mRNA. 12 A post-transcriptional destabilization of c-myc mRNA as a mechanism of type I IFN-mediated c-myc suppression has also been described in colon carcinoma cells. 17 It was shown that, during terminal differentiation of hematopoietic cells, autocrine IFN-b induces c-myc suppression and induces G 0 /G 1 arrest in these cells.…”

Section: Discussionmentioning

confidence: 99%

“…It has been two decades since it was first demonstrated that IFN-b downregulated c-myc expression and this downregulation involved modulation of post-transcriptional control of c-myc mRNA. 11,12 However, the molecules and biochemical pathways involved in this post-transcriptional control remain to be elucidated. We previously demonstrated that hPNPase old-35 was induced very early upon IFN-b treatment and hPNPase old-35 could specifically degrade c-myc mRNA.…”

Section: Introductionmentioning

confidence: 99%

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Defining the mechanism by which IFN-β dowregulates c-myc expression in human melanoma cells: pivotal role for human polynucleotide phosphorylase (hPNPaseold-35)

2006

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Type I interferons (IFN-a/-b) are capable of suppressing c-myc mRNA expression by modulating post-transcriptional processing. However, the molecular mechanism of this phenomenon is poorly understood. We previously established that human polynucleotide phosphorylase (hPNPase old-35 ), a type I IFNinducible 3 0 ,5 0 exoribonuclease involved in mRNA degradation, induces G 1 cell cycle arrest and eventually apoptosis by specifically degrading c-myc mRNA. We now demonstrate a close association between IFN-b-induced hPNPase old-35 upregulation and c-myc downregulation in human melanoma cells. Employing stable melanoma cell clones expressing hPNPase old-35 small inhibitory RNA, we demonstrate that hPNPase old-35 is a key molecule coupled with IFN-b-mediated downregulation of c-myc mRNA. Inhibition of hPNPase old-35 or overexpression of c-myc protects melanoma cells from IFN-bmediated growth inhibition, emphasizing the importance of hPNPase old-35 upregulation and consequent c-myc downregulation in IFN-b-induced growth inhibition and apoptosis induction. In these contexts, targeted overexpression of hPNPase old-35 might be a novel therapeutic strategy for c-myc-overexpressing and IFN-resistant tumors, such as melanomas.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Defining the mechanism by which IFN-β dowregulates c-myc expression in human melanoma cells: pivotal role for human polynucleotide phosphorylase (hPNPaseold-35)

2006

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“…23 and 24, and this study). It has been reported that IFN-␥ stimulates HLA-A2 gene expression 4-to 5-fold at the level of transcription (24,25). However, in such reports, the probe used to assay the level of endogenous HLA-A2 transcription in nuclear run-on assays was a full length HLA-A2 gene that shares large hybridizable stretches of sequence with HLA-B and -C genes (26).…”

mentioning

confidence: 96%

A 3′-Transcribed Region of the HLA-A2 Gene Mediates Posttranscriptional Stimulation by IFN-γ

Snyder

Waring

Sheng

et al. 2001

The Journal of Immunology

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The expression of several MHC class I genes is up-regulated at the transcriptional level by IFN-γ. Posttranscriptional mechanisms also have been implicated, but not well characterized. To investigate the mechanism of IFN-γ stimulation of the human MHC class I gene HLA-A2, several human tumor cell lines were transfected with reporter gene constructs driven by the HLA-A2 promoter. We have previously shown that the extended 525-bp HLA-A2 promoter alone, which includes a 5′ IFN-stimulated response element consensus sequence, is not sufficient for IFN-γ response in either K562 or Jurkat cells. In the current study, stable transfection of a genomic HLA-A2 gene construct, containing both 5′- and 3′-flanking sequences, resulted in stimulation of the gene by IFN-γ. Nuclear run-on assays revealed that, unlike other class I genes, IFN-γ stimulation of HLA-A mRNA accumulation occurs almost entirely through posttranscriptional mechanisms. RNA stability assays showed that the effect is not mediated by alteration of the half-life of the HLA-A2 mRNA. Formation of the 3′ end was unaffected by IFN-γ treatment. Sequences that mediate the majority of IFN-γ induction of HLA-A2 mRNA reside in a 127-bp 3′-transcribed region of the gene. This region contains the terminal splice site, the usage of which is not affected by IFN-γ treatment. These results demonstrate a novel posttranscriptional mechanism of regulation of MHC class I genes by IFN-γ.

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“…It is well documented that c-myc gene expression can be regulated at the level of mRNA stability (8,9). The disappearance of c-myc mRNA in the WEHI 231 cells following 2 h of GaMIg treatment is rapid, occurring with a half-time of less than 30 min.…”

mentioning

confidence: 98%

Transcriptional and posttranscriptional control of c-myc gene expression in WEHI 231 cells.

Levine¹,

McCormack²,

Buckler³

et al. 1986

Mol. Cell. Biol.

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Incubation of WEHI 231 cells, derived from a murine B-cell lymphoma, with antisera directed against its surface immunoglobulin results in the inhibition of growth within 24 h. Previously, we demonstrated that this treatment selectively affects cytoplasmic levels of c-myc mRNA (J. E. McCormack, V. H. Pepe, R. B. Kent, M. Dean, A. Marshak-Rothstein, and G. E. Sonenshein, Proc. Natl. Acad. Sci. USA 81: [5546][5547][5548][5549][5550] 1984). An initial increase in the cytoplasmic mRNA level is followed by a precipitous drop. We now show that the early increase results from a dramatic increase in the rate of c-myc gene transcription, as well as from partial stabilization of the mRNA in the cytoplasm. The later decrease results from a shutdown in transcription of the c-myc gene and a return to the normal lability of the cytoplasmic c-myc mRNA. Treatment with phorbol ester, like treatment with anti-immunoglobulin sera, inhibited WEHI 231 cell growth and caused similar changes in cytoplasmic c-myc mRNA levels, which can also be related to alterations in c-myc gene transcription. These results indicate that the control of c-myc gene expression in B cells is effected through regulation at multiple levels.

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Increased rate of degradation of c-myc mRNA in interferon-treated Daudi cells.

Cited by 179 publications

References 35 publications

Defining the mechanism by which IFN-β dowregulates c-myc expression in human melanoma cells: pivotal role for human polynucleotide phosphorylase (hPNPaseold-35)

Defining the mechanism by which IFN-β dowregulates c-myc expression in human melanoma cells: pivotal role for human polynucleotide phosphorylase (hPNPaseold-35)

A 3′-Transcribed Region of the HLA-A2 Gene Mediates Posttranscriptional Stimulation by IFN-γ

Transcriptional and posttranscriptional control of c-myc gene expression in WEHI 231 cells.

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