Melanin Reduces Ultraviolet-Induced DNA Damage Formation and Killing Rate in Cultured Human Melanoma Cells

Kobayashi, Nobuhiko; Muramatsu, Tsutomu; Yamashina, Yukio; Shirai, Toshihiko; Ohnishi, Takeo; Mori, Toshio

doi:10.1111/1523-1747.ep12371676

Cited by 94 publications

(68 citation statements)

References 25 publications

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“…1). Low number of dead melanoma cells after UV irradiation found by Kobayashi et al [7] was explained by presence of the intracellular melanin and its role in preventing UV induced cell killing by reducing the formation of DNA damage [7]. The limited access to damaged DNA due to the presence of melanin might be the reason for the delay of melanoma cells response to UV-C irradiation in our study.…”

Section: Resultssupporting

confidence: 49%

The UV-C Induced Cell Death in Human Malignant Melanoma and Normal Fibroblasts

Panek

Wiecheć

2016

Acta Phys. Pol. A

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Differences in cellular death between melanoma (Me45) cells and fibroblasts (CCL-110) were investigated after irradiation with UV-C (1.5-15 J/m 2 ) and incubation for up to 48 h. The role of DNA double strand breaks in this process was assessed. Decrease of the Me45 cells viability began about 6 h after irradiation. The fibroblasts viability negatively correlated with the dose applied, since necrosis within this cell population began immediately after irradiation. The enhanced apoptosis of fibroblasts was observed between 6 and 24 h, while for melanoma cells, high level of apoptotic cells was still detected after 48 h. Statistically significant correlation between the percentage of apoptotic cells and DSBs was estimated for both cell lines. The melanoma cells responded differently to the UV-C radiation than did the fibroblasts. These differences were explained by deficiency of the necrotic processes as well as the delay of apoptotic melanoma response to UV-C damage.

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Section: Resultssupporting

confidence: 49%

The UV-C Induced Cell Death in Human Malignant Melanoma and Normal Fibroblasts

Panek

Wiecheć

2016

Acta Phys. Pol. A

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“…Using this ELISA technique, we compared the induction of CPDs and 6-4PPs in two melanoma cell lines with different levels of pigmentation (48). Those melanoma cells had sufficient melanin such that some was located over nuclei in the path of the incoming UV light, and thus a photoprotective effect of the overlying melanin against DNA damage was expected.…”

Section: Elisamentioning

confidence: 99%

“…In that study, we visualized the formation of CPDs and 6-4PPs as several foci per nucleus in normal human fibro- 3 ) was measured by ELISA with the TDM-2 and 64M-2 antibodies. Each point shows the mean 9 standard deviation (SD) of six determinations (48). Fig.…”

Section: Indirect Immunofluorescence In Cultured Cellsmentioning

confidence: 99%

“…There is increasing interest in the roles of UV-induced DNA damage and/or its repair in pigment cell biology, including their role in melanogenesis (tanning) (45)(46)(47), photoprotection and/or photosensitization by melanin (43,48), melanomagenesis (49), etc. Techniques for the quantitation and visualization of UV-induced DNA damage as described in this review may contribute to a better understanding of DNA damage and its biological consequences.…”

Section: Introductionmentioning

confidence: 99%

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Quantitation and Visualization of Ultraviolet‐Induced DNA Damage Using Specific Antibodies: Application to Pigment Cell Biology

Kobayashi

Katsumi

Imoto

et al. 2001

Pigment Cell Research

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The major types of DNA damage induced by sunlight in the scope. This latter method allows us to reconstruct three-diskin are DNA photoproducts, such as cyclobutane pyrimidine mensional images of nuclei containing DNA photoproducts and to simultaneously examine DNA photoproducts and hisdimers (CPDs), (6-4)photoproducts (6-4PPs) and Dewar isotology in multilayered epidermis. Using those techniques, one mers of 6-4PPs. A sensitive method for quantitating and can determine the induction and repair of these three distinct visualizing each type of DNA photoproduct induced by biologtypes of DNA photoproducts in cultured cells and in the skin ically relevant doses of ultraviolet (UV) or sunlight is essential to characterize DNA photoproducts and their biological efexposed to sublethal or suberythematous doses of UV or solar simulated radiation. As examples of the utility of these techfects. We have established monoclonal antibodies specific for niques and antibodies, we describe the DNA repair kinetics CPDs, 6-4PPs or Dewar isomers. Those antibodies allow one to quantitate photoproducts in DNA purified from cultured following irradiation of human cell nuclei and the photoprotective effect of melanin against DNA photoproducts in cultured cells or from the skin epidermis using an enzyme-linked immunosorbent assay. One can also use those specific antibodpigmented cells and in human epidermis. ies with in situ laser cytometry to visualize and measure DNA

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“…As well, UV irradiation and DNA-damaging carcinogenic chemical agents appear to induce DNA repair systems in mammalian cells (19), consistent with the existence of an SOS-like response analogous to that in yeast. Because melanin is photoprotective in human skin and is generally acknowledged as the body's major defense against photocarcinogenesis (20), acting to inhibit the formation of UV-induced DNA photoproducts (21,22) that give rise to "signature mutations" responsible for skin cancer development (23), enhanced melanogenesis might logically be part of the SOS response in skin.…”

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confidence: 99%

DNA damage enhances melanogenesis.

Eller

Ostrom

Gilchrest

1996

Proc. Natl. Acad. Sci. U.S.A.

262

193

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Although the ability of UV irradiation to induce pigmentation in vivo and in vitro is well documented, the intracellular signals that trigger this response are poorly understood. We have recently shown that increasing DNA repair after irradiation enhances UV-induced melanization. Moreover, addition of small DNA fragments, particularly thymine dinucleotides (pTpT), selected to mimic sequences excised during the repair of UV-induced DNA photoproducts, to unirradiated pigment cells in vitro or to guinea pig skin The prokaryotic response to UV irradiation, the so-called SOS response, is well documented and is now known to include the induction of a set of >20 genes involved in DNA repair and cell survival (reviewed in ref. 1). In this case, the single-stranded DNA generated after UV irradiation interacts with and activates a protease, the Rec A protein (2). Activated Rec A protein then cleaves and inactivates the repressors of specific genes, leading to their induction (2).In eukaryotic cells, the existence of a UV-induced DNA damage-responsive SOS-like system mediated by one common transcription regulator has been the subject of considerable controversy. Although a variety of genes are known to be induced by DNA damage (3-6), many of these genes are also induced by agents such as phorbol esters (3, 7) and by metabolic or oxidative stress (8-10). Because UV irradiation is reported, like phorbol esters, to activate protein kinase C directly (11,12) and to produce oxidative damage through generation of free radicals from membrane lipids and otherThe publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact. extranuclear cellular constituents, it cannot be determined whether the effects of UV are due directly to DNA damage or instead to other impacts on the cell. Indeed, two of the major UV-induced transcription factors, AP-1 and NF-KB, are now thought to initiate their responses at or near the plasma membrane (13,14).Perhaps the best-characterized example of DNA damagespecific gene induction involves a DNA repair enzyme, photolyase, encoded by the PHR1 gene in Saccharomyces cerevisiae (6). This gene is induced by a variety of DNA-damaging agents including UV light, methyl methanesulfonate (MMS) and 4-nitroquinoline 1-oxide (4-NQO). Up-regulation of PHR1 gene transcription is, at least in part, accomplished by the removal of a damage-responsive repressor which binds to a specific site in the 5' region of the gene (15).Another well-studied UV and DNA damage-inducible gene is the mammalian GADD45 gene. This gene is transcriptionally activated not only by UV irradiation but also by ionizing radiation and chemical agents that specifically cause base damage (10, 16). The induction of GADD45 by ionizing radiation is mediated by the p53 tumor suppressor protein and the ataxia telangiectasia gene product (17), but the UV-and base-damage responses are less well understood. ...

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Melanin Reduces Ultraviolet-Induced DNA Damage Formation and Killing Rate in Cultured Human Melanoma Cells

Cited by 94 publications

References 25 publications

The UV-C Induced Cell Death in Human Malignant Melanoma and Normal Fibroblasts

The UV-C Induced Cell Death in Human Malignant Melanoma and Normal Fibroblasts

Quantitation and Visualization of Ultraviolet‐Induced DNA Damage Using Specific Antibodies: Application to Pigment Cell Biology

DNA damage enhances melanogenesis.

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