Melanogenesis stimulation in B16-F10 melanoma cells induces cell cycle alterations, increased ROS levels and a differential expression of proteins as revealed by proteomic analysis

Cunha, Elizabeth Sousa da; Kawahara, Rebeca; Kadowaki, Marina Kimiko; Amstalden, Hudson Gouveia; Noleto, Guilhermina Rodrigues; Cadena, Sílvia Maria Suter Correia; Winnischofer, Sheila Maria Brochado; Martinez, Gláucia Regina

doi:10.1016/j.yexcr.2012.05.019

Cited by 44 publications

(43 citation statements)

References 53 publications

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“…During the same time there was an increase in enzyme activity in sham treatments at day 7 as compared to day 3. This could result from oxidative stress produced as a result of culturing conditions [ 36 ]. Regardless of the increase of tyrosinase activity in sham group, there is a significant increase in tyrosinase activity in visible light treated explants.…”

Section: Discussionmentioning

confidence: 99%

Visible Light Induces Melanogenesis in Human Skin through a Photoadaptive Response

et al. 2015

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Visible light (400–700 nm) lies outside of the spectral range of what photobiologists define as deleterious radiation and as a result few studies have studied the effects of visible light range of wavelengths on skin. This oversight is important considering that during outdoors activities skin is exposed to the full solar spectrum, including visible light, and to multiple exposures at different times and doses. Although the contribution of the UV component of sunlight to skin damage has been established, few studies have examined the effects of non-UV solar radiation on skin physiology in terms of inflammation, and limited information is available regarding the role of visible light on pigmentation. The purpose of this study was to determine the effect of visible light on the pro-pigmentation pathways and melanin formation in skin. Exposure to visible light in ex-vivo and clinical studies demonstrated an induction of pigmentation in skin by visible light. Results showed that a single exposure to visible light induced very little pigmentation whereas multiple exposures with visible light resulted in darker and sustained pigmentation. These findings have potential implications on the management of photo-aggravated pigmentary disorders, the proper use of sunscreens, and the treatment of depigmented lesions.

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Section: Discussionmentioning

confidence: 99%

Visible Light Induces Melanogenesis in Human Skin through a Photoadaptive Response

et al. 2015

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“…Melanin is an important regulator of the balance of reactive oxygen species in melanocytes that could alter response of melanocytes to arsenic and UVR when compared to keratinocytes (Cunha et al, 2012; Jenkins and Grossman, 2013; Suzukawa et al, 2012). In this study, we investigate similarities and differences between purported mechanisms underlying arsenic and UVR-induced DNA damage in these two important target cells within the skin.…”

Section: Introductionmentioning

confidence: 99%

Melanocytes and keratinocytes have distinct and shared responses to ultraviolet radiation and arsenic

2014

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The rise of melanoma incidence in the United States is a growing public health concern. A limited number of epidemiology studies suggest an association between arsenic levels and melanoma risk. Arsenic acts as a co-carcinogen with ultraviolet radiation (UVR) for the development of squamous cell carcinoma and proposed mechanisms include generation of oxidative stress by arsenic and UVR and inhibition of UVR-induced DNA repair by arsenic. In this study, we investigate similarities and differences in response to arsenic and UVR in keratinocytes and melanocytes. Normal melanocytes are markedly more resistant to UVR-induced cytotoxicity than normal keratinocytes, but both cell types are equally sensitive to arsenite. Melanocytes were more resistant to arsenite and UVR stimulation of superoxide production than keratinocytes, but the concentration of arsenite necessary to inhibit the activity of the DNA repair protein poly(ADP-ribose)polymerase and enhance retention of UVR-induced DNA damage was essentially equivalent in both cell types. These findings suggest that although melanocytes are less sensitive than keratinocytes to initial UVR-mediated DNA damage, both of these important target cells in the skin share a mechanism related to arsenic inhibition of DNA repair. These findings suggest that concurrent chronic arsenic exposure could promote retention of unrepaired DNA damage in melanocytes and act as a co-carcinogen in melanoma.

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“…The increased melanin production was accompanied by the increased cell population in the G 0 /G 1 phase (Supporting Figure 9), consistent with the literature reporting a positive correlation between melanogenesis and the G 0 /G 1 phase arrest. 30 Taken together, these results indicate that PD suppresses the B16-F10 cell proliferation by inducing G 0 /G 1 phase arrest and promoting apoptotic cell death.…”

Section: Resultsmentioning

confidence: 67%

Polyethylenimine-Dermatan Sulfate Complex, a Bioactive Biomaterial with Unique Toxicity to CD146-Positive Cancer Cells

Kim

Kwak

et al. 2017

ACS Biomater. Sci. Eng.

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We report unique bioactivity of a polycation-polyanion complex with potential utility for cancer therapy. A complex of disulfide-crosslinked polyethyleneimine (CLPEI), a polycation used for gene complexation, and dermatan sulfate (DS), an anionic polysaccharide to shield excessive cationic charge of the former, has toxicity to a specific group of cancer cell lines, including B16-F10 murine melanoma, A375SM human melanoma, and PC-3 human prostate cancer cells. These CLPEI-DS-sensitive cells express CD146, which binds to the complex via interaction with DS. There is a positive correlation between toxicity and intracellular level of CLPEI, indicating that the CLPEI-DS-sensitivity is attributable to the increased cellular uptake of CLPEI mediated by the DS-CD146 interactions. In vitro studies show that CLPEI-DS complex causes G0/G1 phase arrest and apoptotic cell death. In syngeneic and allograft models of B16-F10 melanoma, CLPEI-DS complex administered with a sub-toxic level of doxorubicin potentiates the chemotherapeutic effect of the drug by loosening tumor tissues. Given the unique toxicity, CLPEI-DS complex may be a useful carrier of gene or chemotherapeutics for the therapy of CD146-positive cancers.

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Melanogenesis stimulation in B16-F10 melanoma cells induces cell cycle alterations, increased ROS levels and a differential expression of proteins as revealed by proteomic analysis

Cited by 44 publications

References 53 publications

Visible Light Induces Melanogenesis in Human Skin through a Photoadaptive Response

Visible Light Induces Melanogenesis in Human Skin through a Photoadaptive Response

Melanocytes and keratinocytes have distinct and shared responses to ultraviolet radiation and arsenic

Polyethylenimine-Dermatan Sulfate Complex, a Bioactive Biomaterial with Unique Toxicity to CD146-Positive Cancer Cells

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