c-myc Oncogene expression inhibits the initiation of myogenic differentiation

Denis, Nicole A. St.; Blanc, Sophie F.; Leibovitch, Marie-Pierre; Nicolaı̈ew, Nathalie; Dautry, François; Raymondjean, Michel; Kruh, Jacques; Kitzis, Alain

doi:10.1016/0014-4827(87)90107-8

Cited by 60 publications

(35 citation statements)

References 28 publications

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“…An unanticipated finding in the present study was the induction of nAchR 6 gene expression in ras-transfected BC3H I and C2 cells after serum withdrawal, which is noteworthy in several respects. First, the presence of nAchR 6 mRNA indicates that activation of c-H-ras does not preclude the appearance of all muscle differentiation products, as might be inferred from previous results (12,18,19,62,63 43,64), and the possibility therefore exists that properties differing, for example, between'ras-and erbB-transfected cells are not inherent to these genes. However, although equivalency of dosage has not been yet established for v-erbB, the ras-transfected BC3H 1 cells contain only a single copy of the activated allele, under the control of its own promoter, and c-H-ras mRNA abundance is increased no more than threefold (18).…”

Section: S--mentioning

confidence: 81%

Dihydropyridine receptor gene expression is regulated by inhibitors of myogenesis and is relatively insensitive to denervation.

Shih

Wathen²,

Marshall³

et al. 1990

J. Clin. Invest.

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To evaluate developmental and physiological signals that may influence expression of the dihydropyridine-sensitive "slow"Ca2" channel, we analyzed dihydropyridine receptor (DHPR) mRNA abundance in mouse skeletal muscle. Using synthetic oligonucleotide probes corresponding to the rabbit skeletal muscle DHPR, a 6.5 kb DHPR transcript was identified in postnatal skeletal muscle and differentiated C2 or BC3H1 myocytes, but not cardiac muscle or brain. DHPR gene expression was reversibly suppressed by 0.4 nM transforming growth factor j%-1 or by transfection with a mutant c-H-ras allele, nominal inhibitors of myogenesis that block the appearance of slow channels and DHPR. In contrast, both BC3HI and C2 myocytes containing the activated ras vector expressed the gene encoding the nicotinic acetylcholine receptor subunit, demonstrating that not all muscle-specific genes are extinguished by ras. Denervation stimulated DHPR gene expression less than 0.6-fold, despite 8-fold upregulation of 5-subunit mRNA and reciprocal effects on the skeletal and cardiac aactin genes. Thus, DHPR gene induction is prevented by inhibitors of other muscle-specific genes, whereas, at most, relatively small changes in DHPR mRNA abundance occur during adaptation to denervation. (J. Clin. Invest. 1990. 85:781-789.) calcium channels * differentiation * MyoDI -oncogenes * skeletal muscle transforming growth factor ,8-1

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Section: S--mentioning

confidence: 81%

Dihydropyridine receptor gene expression is regulated by inhibitors of myogenesis and is relatively insensitive to denervation.

Shih

Wathen²,

Marshall³

et al. 1990

J. Clin. Invest.

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“…We chose to analyse the c-myc gene, which is frequently translocated and/or ampli®ed in tumors (for review, see Marcu et al, 1992;Bishop, 1995), and the DHFR gene, whose genomic instability is altered following either drug selection (Stark, 1993), growth factor (Huang and Wright, 1994) or c-Myc overexpression (Denis et al, 1991;Mai, 1994;Mai et al, 1996). We also examined the CAD and the ribonucleotide reductase R1 (R1) genes.…”

Section: Abnormal Centrosome Ampli®cation In Vivo In P53mentioning

confidence: 99%

“…Moreover, c-Myc overexpression has been implicated in gene ampli®cation (Denis et al, 1991;Mai, 1994;Mai et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Genomic instability and apoptosis are frequent in p53 deficient young mice

et al. 1997

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“…One possible interpretation of our findings is that N-myc expression may be required to expand specific pools of precursor cells by promoting their growth, inhibiting their death, and/or preventing their terminal differentiation. It has been shown that constitutive expression of c-myc can inhibit differentiation of cultured cell lines (Theile et al 1985;Coppola and Cole 1986;Denis et al 1987;Freytag 1988;Larcher et al 1991 ). In addition, it is notable that prelymphocytespecific growth factor, I1-7, induces N-myc in pre-B cells while also inducing proliferation, but not differentiation.…”

Section: Possible Function Of the N-myc Proteinmentioning

confidence: 99%

Embryonic lethality in mice homozygous for a targeted disruption of the N-myc gene.

Charron¹,

Malynn²,

Fisher³

et al. 1992

Genes & Development

293

210

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The N-myc gene encodes a putative transcription factor that is thought to function in the regulation of gene expression during cell differentiation and/or growth. To examine the role of N-myc during development, we have used targeted mutagenesis in embryonic stem cells to produce a mouse line that carries an N-myc null allele. Mice homozygous for the mutation died between 10.5 and 12.5 days of gestation. Histological analysis of mutant embryos revealed that organs and tissues expected at these stages of development were present. However, multiple defects were observed, primarily in tissues and organs that normally express N-myc. In particular, mutant hearts were underdeveloped, often retaining the S-shape more typical of 9-day-old embryos. In addition, cranial and spinal ganglia were reduced in size and/or cellularity. Most of the noted defects were more consistent with a role of N-myc in proliferation of precursor populations than with a block in differentiation per se, at least at these early stages. These results demonstrate that N-myc plays an essential role during development and clearly confirm that N-myc has a physiological function that is distinct from that of the other myc-family genes.

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c-myc Oncogene expression inhibits the initiation of myogenic differentiation

Cited by 60 publications

References 28 publications

Dihydropyridine receptor gene expression is regulated by inhibitors of myogenesis and is relatively insensitive to denervation.

Dihydropyridine receptor gene expression is regulated by inhibitors of myogenesis and is relatively insensitive to denervation.

Genomic instability and apoptosis are frequent in p53 deficient young mice

Embryonic lethality in mice homozygous for a targeted disruption of the N-myc gene.

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