Human 8-oxoguanine-DNA glycosylase-1 is downregulated in human basal cell carcinoma

Huang, Xiaoshui; Scolyer, Richard A.; Abubakar, Askar; Halliday, Gary M.

doi:10.1016/j.ymgme.2012.02.017

Cited by 24 publications

(17 citation statements)

References 24 publications

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“…As shown above, miR-23b is increased in expression with a factor of +6.8 after UVA-irradiation which is known to be an important risk factor for developing non-melanocytic skin cancers (NMSCs), like BCC [49], [50].…”

Section: Resultsmentioning

confidence: 92%

UVA and UVB Irradiation Differentially Regulate microRNA Expression in Human Primary Keratinocytes

et al. 2013

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MicroRNA (miRNA)-mediated regulation of the cellular transcriptome is an important epigenetic mechanism for fine-tuning regulatory pathways. These include processes related to skin cancer development, progression and metastasis. However, little is known about the role of microRNA as an intermediary in the carcinogenic processes following exposure to UV-radiation. We now show that UV irradiation of human primary keratinocytes modulates the expression of several cellular miRNAs. A common set of miRNAs was influenced by exposure to both UVA and UVB. However, each wavelength band also activated a distinct subset of miRNAs. Common sets of UVA- and UVB-regulated miRNAs harbor the regulatory elements GLYCA-nTRE, GATA-1-undefined-site-13 or Hox-2.3-undefined-site-2 in their promoters. In silico analysis indicates that the differentially expressed miRNAs responding to UV have potential functions in the cellular pathways of cell growth and proliferation. Interestingly, the expression of miR-23b, which is a differentiation marker of human keratinocytes, is remarkably up-regulated after UVA irradiation. Studying the interaction between miR-23b and its putative skin-relevant targets using a Luciferase reporter assay revealed that RRAS2 (related RAS viral oncogene homolog 2), which is strongly expressed in highly aggressive malignant skin cancer, to be a direct target of miR-23b. This study demonstrates for the first time a differential miRNA response to UVA and UVB in human primary keratinocytes. This suggests that selective regulation of signaling pathways occurs in response to different UV energies. This may shed new light on miRNA-regulated carcinogenic processes involved in UV-induced skin carcinogenesis.

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Section: Resultsmentioning

confidence: 92%

UVA and UVB Irradiation Differentially Regulate microRNA Expression in Human Primary Keratinocytes

et al. 2013

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“…The hOGG1 protein initiates the base excision repair (BER) pathway by recognizing and excising the modified base by hydrolyzing the N-glycosidic bond. 8-OH-G is one of the major pre-mutagenic derivatives of the DNA bases, resulting from the exposure to reactive oxygen species (ROS), and it has been used as a biomarker for cellular oxidative stress [59]. 8-OH-G can pair with adenine in double-stranded DNA during the DNA replication leading to a G:C to T:A transversion.…”

Section: Hogg1mentioning

confidence: 99%

“…Since c.977C>G is located in the coding region of the hOGG1 gene it may directly affect protein stability and function. It has been demonstrated that this SNP can be associated with an increased risk of lung, esophagus, prostate and a subset of stomach cancers [59,62–64]. …”

Section: Hogg1mentioning

confidence: 99%

Genetic Variability in DNA Repair Proteins in Age-Related Macular Degeneration

Błasiak

Synowiec

Salminen

2012

IJMS

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The pathogenesis of age-related macular degeneration (AMD) is complex and involves interactions between environmental and genetic factors, with oxidative stress playing an important role inducing damage in biomolecules, including DNA. Therefore, genetic variability in the components of DNA repair systems may influence the ability of the cell to cope with oxidative stress and in this way contribute to the pathogenesis of AMD. However, few reports have been published on this subject so far. We demonstrated that the c.977C>G polymorphism (rs1052133) in the hOGG1 gene and the c.972G>C polymorphism (rs3219489) in the MUTYH gene, the products of which play important roles in the repair of oxidatively damaged DNA, might be associated with the risk of AMD. Oxidative stress may promote misincorporation of uracil into DNA, where it is targeted by several DNA glycosylases. We observed that the g.4235T>C (rs2337395) and c.–32A>G (rs3087404) polymorphisms in two genes encoding such glycosylases, UNG and SMUG1, respectively, could be associated with the occurrence of AMD. Polymorphisms in some other DNA repair genes, including XPD (ERCC2), XRCC1 and ERCC6 (CSB) have also been reported to be associated with AMD. These data confirm the importance of the cellular reaction to DNA damage, and this may be influenced by variability in DNA repair genes, in AMD pathogenesis.

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“…Human 8-oxoguanine-DNA glycosylase 1 (HOGG1) is the main enzyme that excises 8-oxo-dG from damaged DNA via the base-excision repair pathway. [61] Furthermore, basal cells in human epidermis are particularly sensitive to UVA-mediated DNA damage probably due to low expression of HOGG1. [62] In this study, we observed increased HOGG1 (human ogg1) in acute UVB-exposed HDFa.…”

Section: Discussionmentioning

confidence: 99%

Ferulic acid prevents ultraviolet-B radiation induced oxidative DNA damage in human dermal fibroblasts

Ambothi

Prasad

2014

Int J Nutr Pharmacol Neurol Dis

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Aim: Protective effects of ferulic acid (FA) against ultraviolet-B (290-320 nm) radiation induced cellular changes were investigated in human dermal fibroblasts (HDFa). Materials and Methods: HDFa cells pretreated with increasing concentrations of FA (0, 10, 20, 40 μg/ml) for 30 min, were UVB irradiated and different cellular and oxidative end points were analyzed. Results: The percentage of cytotoxicity, intracellular reactive oxygen species (ROS) levels, mitochondrial membrane potential, thiobarbituric acid reactive substances (TBARS) and DNA damage, were significantly increased in 19.8 mJ/cm 2 ultraviolet-B (UVB)-exposed HDFa. Further, exposure to UVB causes significantly decreased antioxidants status in HDFa cells. Treatment of HDFa cells with FA before 30 min of UVB-irradiation significantly restored mitochondrial membrane potential, ROS levels and antioxidant status in HDFa. Further, FA treatment reverted UVB-induced mutagenesis in Ames tester strains and DNA damage in HDFa. Moreover, we noticed increased expression of GADD 45, XRCC1 and HOGG1 in UVB exposed HDFa. Conversely, FA pretreatment significantly attenuated UVB-induced expression of DNA repair genes in HDFa. Conclusion: The present findings indicate that FA act as a sunscreen rather than working at molecular level to offer photoprotection.

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Human 8-oxoguanine-DNA glycosylase-1 is downregulated in human basal cell carcinoma

Cited by 24 publications

References 24 publications

UVA and UVB Irradiation Differentially Regulate microRNA Expression in Human Primary Keratinocytes

UVA and UVB Irradiation Differentially Regulate microRNA Expression in Human Primary Keratinocytes

Genetic Variability in DNA Repair Proteins in Age-Related Macular Degeneration

Ferulic acid prevents ultraviolet-B radiation induced oxidative DNA damage in human dermal fibroblasts

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