XPC: Going where no DNA damage sensor has gone before

Nemzow, Leah; Lubin, Abigail; Zhang, Ling; Gong, Feng

doi:10.1016/j.dnarep.2015.09.004

Cited by 28 publications

(18 citation statements)

References 92 publications

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“…Its encoding protein consists of 940 amino acids and acts as a DNA damage recognition molecule during the global genome NER pathway [43,44]. XPC can bind tightly with RAD23 homolog B (RAD23B, also called HR23B) to form a stable XPC/RAD23B complex.…”

Section: Xeroderma Pigmentosum C (Xpc) Gsnps and Afb1-hcc Among Guangmentioning

confidence: 99%

“…XPC can bind tightly with RAD23 homolog B (RAD23B, also called HR23B) to form a stable XPC/RAD23B complex. This complex can recognize DNA adducts formed by exogenous carcinogens such as AFB1 and binds to the DNA damage sites [44]. Thus, XPC may play a role in the pathogenesis of HCC-related AFB1.…”

Section: Xeroderma Pigmentosum C (Xpc) Gsnps and Afb1-hcc Among Guangmentioning

confidence: 99%

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Genetic Single Nucleotide Polymorphisms (GSNPs) in the DNA Repair Genes and Hepatocellular Carcinoma Related to Aflatoxin B1 among Guangxiese Population

Wu¹,

Xi²,

Lü³

et al. 2017

Genetic Polymorphisms

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Alatoxin B1 (AFB1) is an important environmental carcinogen for the development of hepatocellular carcinoma (HCC). HCC is a complex disease likely resulting from genetic single nucleotide polymorphisms (GSNPs) of multiple interacting genes and geneenvironment interactions. Recent eforts have been made to analyze the associations between risk of this malignancy and GSNPs in genes involved in the repair of DNA damage induced by AFB1. Here, we reviewed the results of published case-control studies that have examined the efects of common alleles of all susceptible DNA repair genes, including XRCC1, XRCC3, XRCC4, XRCC7, XPC, and XPD, on risk of AFB1-related HCC among Guangxi population. Statistically signiicant diferences in genotype frequencies found in case-control comparisons were rs25487, rs80309960, rs861539, rs7003908, rs28383151, rs3734091, rs13181, and rs2228001 polymorphism. The overall efects of these GNSPs were moderate in terms of relative risk, with ORs ranging from 2 to 10. Furthermore, some evidence of the interaction of GSNPs in DNA repair genes and AFB1 exposure modulate risk of this cancer was also found, although the results require conirmation with larger sample size studies.

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Section: Xeroderma Pigmentosum C (Xpc) Gsnps and Afb1-hcc Among Guangmentioning

confidence: 99%

Section: Xeroderma Pigmentosum C (Xpc) Gsnps and Afb1-hcc Among Guangmentioning

confidence: 99%

Genetic Single Nucleotide Polymorphisms (GSNPs) in the DNA Repair Genes and Hepatocellular Carcinoma Related to Aflatoxin B1 among Guangxiese Population

Wu¹,

Xi²,

Lü³

et al. 2017

Genetic Polymorphisms

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show abstract

“…[45][46][47][48] In this context, it is important to mention that BER is a basic repair mechanism for the mitochondrial DNA (mtDNA). Investigating the connection between repair and metabolism, Rezvani et al performed a knockdown of the XPC protein, which is also involved in BER, [49,50] and observed deficiencies in mitochondrial bioenergetics [47,51] with decreased mitochondrial ATP levels and increased glycolysis parallel to increased ROS levels and increased nuclear and mitochondrial oxidative DNA damage. The authors propose that the enhanced mutagenesis especially in mtDNA decreases oxidative phosphorylation, which decreases the cellular energy level.…”

Section: The Immed Iate Effec Ts Of U Va Damag E and Its Me Taboli mentioning

confidence: 99%

UVA, metabolism and melanoma: UVA makes melanoma hungry for metastasis

Kamenisch

Ivanova

Drexler

et al. 2018

Experimental Dermatology

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Ultraviolet (UV) radiation has a plethora of effects on human tissues. In the UV spectrum, wavelengths above 320 nm fall into the UVA range, and for these, it has been shown that they induce reactive oxygen species (ROS), DNA mutations and are capable to induce melanoma in mice. In addition to this, it was recently shown that UVA irradiation and UVA-induced ROS also increase glucose metabolism of melanoma cells. UVA irradiation causes a persistent increase in glucose consumption, accompanied by increased glycolysis, increased lactic acid production and activation of the pentose phosphate pathway. Furthermore, it was shown that the enhanced secretion of lactic acid is important for invasion of melanoma in vitro. The current knowledge of this link between UVA, metabolism and melanoma, possible mechanisms of UVA-induced glucose metabolism and their starting points are discussed in this review with focus on ROS- and UVA-induced cellular stress signalling, DNA damage signalling and DNA repair systems. When looking at the benefits of UVA-induced glucose metabolism, it becomes apparent that there are more advantages of these metabolic changes than one would expect. Besides the role of lactic acid as initiator of protease expression and invasion, its role for immune escape of melanoma cells and the pentose phosphate pathway-derived nicotinamide adenine dinucleotide phosphate (NADPH) as part of a ROS detoxification strategy are discussed.

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“…Depletion of TDG in ESCs leads to ectopic 5fC and 5caC signals at active gene enhancers bound by pluripotency transcription factors, suggesting that, despite a lack of sequence specificity, TDG may be recruited to these regulatory sites to maintain a hypomethylated state by an unknown mechanism. Interestingly, the XPC DNA repair complex, a DNA damage sensor in nucleotide exci-sion repair (Nemzow et al 2015), was shown recently to function as a critical transcriptional coactivator for stem cell-specific transcription factors OCT4 and SOX2 (Fong et al 2011). Similar to TDG, the XPC complex occupies both distal enhancers and promoters that are also bound by OCT4, SOX2, and potentially other transcription factors expressed in ESCs (Cattoglio et al 2015).…”

mentioning

confidence: 99%

Regulation of DNA demethylation by the XPC DNA repair complex in somatic and pluripotent stem cells

Cattoglio

McSwiggen

et al. 2017

Genes Dev.

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Faithful resetting of the epigenetic memory of a somatic cell to a pluripotent state during cellular reprogramming requires DNA methylation to silence somatic gene expression and dynamic DNA demethylation to activate pluripotency gene transcription. The removal of methylated cytosines requires the base excision repair enzyme TDG, but the mechanism by which TDG-dependent DNA demethylation occurs in a rapid and site-specific manner remains unclear. Here we show that the XPC DNA repair complex is a potent accelerator of global and locus-specific DNA demethylation in somatic and pluripotent stem cells. XPC cooperates with TDG genome-wide to stimulate the turnover of essential intermediates by overcoming slow TDG-abasic product dissociation during active DNA demethylation. We further establish that DNA demethylation induced by XPC expression in somatic cells overcomes an early epigenetic barrier in cellular reprogramming and facilitates the generation of more robust induced pluripotent stem cells, characterized by enhanced pluripotency-associated gene expression and self-renewal capacity. Taken together with our previous studies establishing the XPC complex as a transcriptional coactivator, our findings underscore two distinct but complementary mechanisms by which XPC influences gene regulation by coordinating efficient TDG-mediated DNA demethylation along with active transcription during somatic cell reprogramming.

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XPC: Going where no DNA damage sensor has gone before

Cited by 28 publications

References 92 publications

Genetic Single Nucleotide Polymorphisms (GSNPs) in the DNA Repair Genes and Hepatocellular Carcinoma Related to Aflatoxin B1 among Guangxiese Population

Genetic Single Nucleotide Polymorphisms (GSNPs) in the DNA Repair Genes and Hepatocellular Carcinoma Related to Aflatoxin B1 among Guangxiese Population

UVA, metabolism and melanoma: UVA makes melanoma hungry for metastasis

Regulation of DNA demethylation by the XPC DNA repair complex in somatic and pluripotent stem cells

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