Nucleotide sequence of the human c-myc locus: provocative open reading frame within the first exon.

Gazin, Claude; Dinechin, S. Dupont de; Hampe, A; Masson, Jean-Daniel; Martin, Patrick; Stéhelin, D; Galibert, Francis

doi:10.1002/j.1460-2075.1984.tb01816.x

Cited by 203 publications

(121 citation statements)

References 32 publications

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“…In order to quantify and to localize more precisely the new site induced in c-myc, the autoradiogram shown in [22]. The analysis also indicated that the intensity of cleavage induced by mAMSA at position +3100 was equal to 19.5% and 3.5% of the total c-myc gene cleavage generated for differentiated or undifferentiated HL60 cells, respectively.…”

Section: Resultsmentioning

confidence: 99%

Analysis of topoisomerase II‐mediated DNA cleavage of the c‐myc gene during HL60 differentiation

1993

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We have investigated the effect of mAMSA, a potent topoisomerase II inhibitor, on the c-myc proto-oncogene of the acute promyelocytic leukemia HL60 cell line during its differentiation. When HL60 cells were induced by dimethylsulfoxide (DMSO) to terminally differentiate, a rapid drop m the level of c-myc mRNA was observed, followed by an arrest of cell proliferation. In contrast, the level of topoisomerase II mRNA was transiently Increased with a maximum at 6 h after DMSO addition and was then completely abolished after 48 h, indicating that topoisomerase II is activated during the onset of HL60 differentiation. In exponentially growing cells, treatment by mAMSA results in the formation of topoisomerase II-mediated double strand DNA breaks in the c-myc gene at positions where topoisomerase II would normally nick and reseal the two strands. In HL60 cells treated with both mAMSA and DMSO, the sites in the c-myc gene at which mAMSA had induced cleavage were not altered. However, a DNA cleavage site located at the end of the first c-myc exon (position +3100), was strongly stimulated by mAMSA and DMSO treatment. This site fell within a DNase I hypersensitive region encompassing the MYC intron factor 1 (MIFl) binding site, where transcription elongation is normally blocked during differentiation. These data indicate that a change of topoisomerase II binding to critical regulatory region of the c-myc gene is associated with the downregulation of this gene during differentiation.

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Section: Resultsmentioning

confidence: 99%

Analysis of topoisomerase II‐mediated DNA cleavage of the c‐myc gene during HL60 differentiation

1993

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“…The hTIC-myc plasmid was generated by sticky and blunt end ligation, respectively, of the hTIC XbaI and SphI sites to a 4575 bp XbaI/EcoRI gene fragment of the human c-myc gene. This fragment spans nt 3507-8082 (Gazin et al, 1984) and includes the complete c-myc exon 2/3 region and second intron with the preferred ATG start codon in exon 2, plus a portion of intron one. It does not contain the weak alternative translation start site found in exon 1 (Gazin et al, 1984) and only p62 Myc protein can be produced.…”

Section: Generation Of Rodent ®Broblast Cell Lines Stably Transfectedmentioning

confidence: 99%

“…This fragment spans nt 3507-8082 (Gazin et al, 1984) and includes the complete c-myc exon 2/3 region and second intron with the preferred ATG start codon in exon 2, plus a portion of intron one. It does not contain the weak alternative translation start site found in exon 1 (Gazin et al, 1984) and only p62 Myc protein can be produced. The hTIC-myc plasmid was linearized at a unique FspI restriction enzyme site before transfection.…”

Section: Generation Of Rodent ®Broblast Cell Lines Stably Transfectedmentioning

confidence: 99%

“…The pelleted RNA was resuspended in diethyl pyrocarbonate-treated H 2 O and 10 ± 20 mg were run on a 1% agarose/ 2 M formaldehyde gel. The electrophoretically-separated RNA was transferred to Zetaprobe GT (Biorad) membrane, UV-crosslinked and hybridized to a 416 bp PstI human c-myc exon 2 gene fragment (Gazin et al, 1984) as described (Helbing et al, 1996).…”

Section: Rna Isolation and Northern Blot Analysesmentioning

confidence: 99%

“…These primers span the second intron of the c-myc gene to enable detection of any contaminating genomic DNA in cDNA preparations. Both endogenous rat and exogenous human c-myc transcripts are ampli®ed because the human c-myc gene (Gazin et al, 1984) di ers from the rat by only one nucleotide in primer ME2/3-1 and 2 nucleotides in the 5' end of primer ME2/3-2. Polymerase chain reactions were performed as described previously (Helbing et al, 1996) using 30 cycles of 20 s at 948C, 1 min at 588C and 1 min at 728C.…”

Section: Rt-pcr Analysesmentioning

confidence: 99%

See 2 more Smart Citations

Quiescence versus apoptosis: Myc abundance determines pathway of exit from the cell cycle

et al. 1998

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Overexpression of humanmutT homologue gene messenger RNA in renal-cell carcinoma: Evidence of persistent oxidative stress in cancer

et al. 1996

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Data regarding oxidatively modified DNA bases suggest that cancer cells are more exposed to oxidative stress than adjacent non-tumorous tissue. This novel concept may contribute to the understanding of certain aspects of tumor biology such as activated transcription factors, genetic instability, chemotherapy-resistance and metastasis. We therefore tested this concept in human renal-cell carcinomas (RCCs) by evaluating the expression of hMTH1, an enzyme preventing the misincorporation into DNA of 8-0x0-dGTP (8-oxo-7,8-dihydrodeoxyguanosine triphosphate), an oxidized form of dGTP in the nucleotide pool. The expression of hMTHl messenger RNA (mRNA) in RCC was significantly higher than that in adjacent nontumorous kidney. Moreover, advanced-stage tumors showed significantly higher hMTHl mRNA expression than early-stage tumors, and there was a modest linear correlation between hMTHl expression and c-myc expression. The results provide logical support for the concept of "persistent oxidative stress in cancer" and suggest a role of hMTHl mRNA level as a prognostic marker.o 1996 Wiley-Liss, Inc.It is generally accepted that reactive oxygen species (ROS) play a role in carcinogenesis by inducing mutagenic modifications in DNA (Halliwell and Gutteridge, 1989; Halliwell and Aruoma, 1993). However, ROS in tumor biology is a research area not intensively investigated so far. We recently measured in human renal-cell carcinoma (RCC) the amount of 8-0x0-2'-deoxyguanosine (8-0x0-dG, also called 8-hydroxy-2'-deoxyguanosine), a mutation-prone DNA base created by ROS (hydroxyl radical, singlet oxygen or direct photodynamic action) (Kasai and Nishimura, 1984; Kasai et al., 1992; Halliwell and Aruoma, 1993), and found significantly higher levels of 8-0x0-dG in RCC than in adjacent non-tumorous tissue at various stages of the disease (Okamoto et al., 1994). Based on our study and those of others, we hypothesized a concept of "persistent oxidative stress in cancer" that may contribute to aspects of tumor biology such as activated transcription factors and proto-oncogenes, genetic instability, chemotherapyresistance and metastasis (Toyokuni et al., 1995). A study was undertaken to test this hypothesis.At least 2 different metabolic pathways for the presence of 8-0x0-dG in DNA have been established (1) direct hydroxylation of C-8 of dG in DNA that causes a G:C to T A transversion upon replication (Kuchino et al

show abstract

Nucleotide sequence of the human c-myc locus: provocative open reading frame within the first exon.

Cited by 203 publications

References 32 publications

Analysis of topoisomerase II‐mediated DNA cleavage of the c‐myc gene during HL60 differentiation

Analysis of topoisomerase II‐mediated DNA cleavage of the c‐myc gene during HL60 differentiation

Quiescence versus apoptosis: Myc abundance determines pathway of exit from the cell cycle

Overexpression of humanmutT homologue gene messenger RNA in renal-cell carcinoma: Evidence of persistent oxidative stress in cancer

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