The potential roles of p53 tumor suppressor in nucleotide excision repair (NER) and base excision repair (BER)

Seo, Young Rok; Jung, Hwa Jin

doi:10.1038/emm.2004.64

Cited by 51 publications

(38 citation statements)

References 37 publications

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“…Figure 6 Suggested model for a role of the Gadd45a and apurinic/apyrimidinic endonuclease 1/redox factor 1 (APE1/Ref1) in the base excision repair (BER) response. Several reports have shown a role for p53 protein by directly interacting with DNA polymerase b in BER (Zhou et al, 2001;Offer et al, 2001;Seo et al, 2002a;Seo and Jung, 2004). In this study, we suggest an alternative pathway that gadd45a as one of p53 downstream genes might also play a role in the enhancement of BER by modulation of localization of APE1/Ref1, which is known to involve BER as well as to activate p53.…”

Section: Detection Of Ap Sitessupporting

confidence: 58%

“…Several groups including ours have shown that the p53 tumor suppressor protein regulates BER (Offer et al, 2001;Zhou et al, 2001;Seo et al, 2002a;Seo and Jung, 2004). In particular, p53-null cells exhibited defective BER, which was attributed to direct interaction of p53 protein with the DNA polymerase b enzyme required for BER (Zhou et al, 2001).…”

Section: Introductionmentioning

confidence: 82%

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Base excision DNA repair defect in Gadd45a-deficient cells

et al. 2007

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Section: Detection Of Ap Sitessupporting

confidence: 58%

Section: Introductionmentioning

confidence: 82%

Base excision DNA repair defect in Gadd45a-deficient cells

et al. 2007

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“…[14][15][16][53][54][55][56][57] It was, therefore, of interest to look for a possible variation in the functional status of p53 in the T-cell lines employed in this study that might explain the different patterns of Tax effects on NER in these cells. Although several laboratories claim that Jurkat cells are p53 null, we have previously shown that the Jurkat cells used in our experiments, express comparable levels of both w.t.…”

Section: Tax Effect On Ner In Human T-cellsmentioning

confidence: 99%

Retracted: Dose‐dependent dual effect of HTLV‐1 tax oncoprotein on p53‐dependent nucleotide excision repair in human T‐cells

Schavinsky-Khrapunsky¹,

Priel²,

Aboud³

2007

Intl Journal of Cancer

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In this study we investigated the effect of Tax on nucleotide excision repair (NER) in human T-cell lines by using the host cell repair analysis of UVC-irradiated reporter plasmid. This analysis revealed a p53-dpendent NER activity in wild type (w.t.) p53-containing T-cells and p53-independent NER in w.t. p53-lacking Tcells. Notably, in the w.t. p53-containing cells Tax exerted a dosedependent dual effect on NER. While low Tax doses markedly stimulated this repair, high Tax doses strongly reduced it. Further experiments demonstrated that the low Tax doses enhanced, in these cells, the level and the transcriptional function of their w.t. p53 protein. On the other hand, although the high Tax doses further increased the level of p53, they functionally inactivated its accumulating molecules. Both of these Tax effects on p53 proved to be mediated by Tax-induced NF-jB-related mechanisms. Together, these data suggest that by NF-jB activation Tax elevates the level of the cellular w.t. p53. However, while at low Tax doses the elevating w.t. p53 molecules are functionally active and capable of stimulating NER, intensifying further the NF-jB activation by the high Tax doses concomitantly evokes certain mechanism(s) which functionally inactivates the accumulating p53 protein. In contrast to this dual effect on the p53-dependent NER, Tax displayed only an inhibitory effect on the p53-independent NER by its high doses, whereas its low doses had no effect on this repair. The mechanisms of the NF-jB-associated effects on the level and function of the cellular w.t.p53 and of the p53-independent NER noted in our experimental systems are further investigated in our laboratory. ' 2007 Wiley-Liss, Inc.

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“…However, 90% of mutations are clustered between exons 5 and 8 in four conserved regions of the p53 gene. Another possibility is the binding of the wild-type p53 protein to other proteins, such as MDM2 or E6 viral oncoprotein, stabilizes and inactivates as a result of the over expression (Barenes et al, 1992;Momand et al, 1992;Cho et al, 2002;Seo et al, 2004). The results of PCR-SSCP followed by direct DNA sequencing and immunoblotting demonstrated p53 gene mutations associated with abnormal accumulation of p53 protein in OSC cell lines.…”

Section: Discussionmentioning

confidence: 99%

Characterization of newly established oral cancer cell lines derived from six squamous cell carcinoma and two mucoepidermoid carcinoma cells

Lee

Kim²,

Lee³

et al. 2005

Exp Mol Med

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Since genetic abnormalities of human cancer are greatly geographically dependent, cultural and environmental backgrounds are thought to be closely related to the carcinogenic process. In the present study, eight human cell lines were established by culture from untreated carcinomas of the oral cancer, of which five were from primary oral squamous cell carcinomas (OSC), one from a mucoepidermoid carcinoma (MEC) and one each originating from metastatic OSC and MEC. All the studied tumor lines grew as monolayers, and showed: i) an epithelial origin by the presence of cytokeratin, and ii) tumorigenic potential in nude mice. Western blot analysis revealed i) over expression of EGFR in six of the cell lines ii) decreased expression of Ecadherin in six cell lines compared to normal human oral mucosa. A mutational analysis showed: point mutations of p53 at exon 7, with transversion, and at exon 8, with transition. These well-characterized human YD cell lines should serve as useful tools in the study of the molecular pathogenesis and biological characteristics of head and neck cancer cells, and in the future testing of new therapeutic reagents for oral cancer.

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The potential roles of p53 tumor suppressor in nucleotide excision repair (NER) and base excision repair (BER)

Abstract: Abbreviations: AP endonuclease, apurinic/apyrimidinic endonuclease; BER, base excision repair; MMS, methyl methanesulfonate; NER, nucleotide excision repair; PCNA, proliferating cell nuclear antigen; β-pol, DNA polymerase beta

Cited by 51 publications

References 37 publications

Base excision DNA repair defect in Gadd45a-deficient cells

Base excision DNA repair defect in Gadd45a-deficient cells

Retracted: Dose‐dependent dual effect of HTLV‐1 tax oncoprotein on p53‐dependent nucleotide excision repair in human T‐cells

Characterization of newly established oral cancer cell lines derived from six squamous cell carcinoma and two mucoepidermoid carcinoma cells

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