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Silibinin and non-melanoma skin cancers.

ABSTRACT: Skin is the largest human organ that shields the inner body from contact with xenobiotic and genotoxic agents, and in this process, the skin's cellular genome faces continuous stress due to direct exposure to these noxious factors. Accumulation of genetic stress results in genomic alterations leading to undesirable gene or protein alteration/expression in skin cells, which eventually causes the formation of non-melanoma skin cancers (NMSCs). Ultraviolet B (UVB) radiation from sun is the most prominent factor contributing to ?5 million skin cancer cases (which are mostly NMSCs) in the United States (US) and western countries. UVB exposure causes aberrations in a range of biochemical and molecular pathways such as: thymine dimer formation, DNA damage, oxidative stress, inflammatory responses, altered cellular signaling, which ultimately contribute to the development of NMSCs. The focus of this review is to summarize the protective and preventive potential of silymarin and/or silibinin against UVB-induced NMSC in pre-clinical skin cancer studies. Over two decades of research has shown the strong potential of silibinin, a biologically active flavonolignan (crude form Silymarin) derived from milk thistle plant, against a wide range of cancers, including NMSCs. Silibinin protects against UVB-induced thymine dimer formation and in turn promotes DNA repair and/or initiates apoptosis in damaged cells via an increase in p53 levels. Additionally, silibinin has shown strong efficacy against NMSCs via its potential to target aberrant signaling pathways, and induction of anti-inflammatory responses. Overall, completed comprehensive studies suggest the potential use of silibinin to prevent and/or manage NMSCs in humans.

SUBMITTER: Prasad RR

PROVIDER: S-EPMC7340873 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature

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Silibinin and non-melanoma skin cancers.

Prasad Ram Raj RR Paudel Sandeep S Raina Komal K Agarwal Rajesh R

Journal of traditional and complementary medicine 20200206 3

Skin is the largest human organ that shields the inner body from contact with xenobiotic and genotoxic agents, and in this process, the skin's cellular genome faces continuous stress due to direct exposure to these noxious factors. Accumulation of genetic stress results in genomic alterations leading to undesirable gene or protein alteration/expression in skin cells, which eventually causes the formation of non-melanoma skin cancers (NMSCs). Ultraviolet B (UVB) radiation from sun is the most pro ...[more]

PMID: 32670818

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Project description:BackgroundThe Grainyhead-like (GRHL) transcription factors have been linked to many different types of cancer. However, no previous study has attempted to investigate potential correlations in expression of different GRHL genes in this context. Furthermore, there is very little information concerning damaging mutations and/or single nucleotide polymorphisms in GRHL genes that may be linked to cancer.MethodsDNA and RNA were extracted from human non-melanoma skin cancers (NMSC) and adjacent normal tissues (n = 33 pairs of samples). The expression of GRHL genes was measured by quantitative real time PCR. Regulation of GRHL expression by miRNA was studied using cell transfection methods and dual-luciferase reporter system. Targeted deep sequencing of GRHL genes in tumor samples and control tissues were employed to search for mutations and single nucleotide polymorphisms. Single marker rs141193530 was genotyped with pyrosequencing in additional NMSC replication cohort (n = 176). Appropriate statistical and bioinformatic methods were used to analyze and interpret results.ResultsWe discovered that the expression of two genes - GRHL1 and GRHL3 - is reduced in a coordinated manner in tumor samples, in comparison to the control healthy skin samples obtained from the same individuals. It is possible that both GRHL1 and GRHL3 are regulated, at least to some extent, by different strands of the same oncogenic microRNA - miR-21, what would at least partially explain observed correlation. No de novo mutations in the GRHL genes were detected in the examined tumor samples. However, some single nucleotide polymorphisms in the GRHL genes occur at significantly altered frequencies in the examined group of NMSC patients.ConclusionsNon-melanoma skin cancer growth is accompanied by coordinated reduced expression of epidermal differentiation genes: GRHL1 and GRHL3, which may be regulated by miR-21-3p and -5p, respectively. Some potentially damaging single nucleotide polymorphisms in GRHL genes occur with altered frequencies in NMSC patients, and they may in particular impair the expression of GRHL3 gene or functioning of encoded protein. The presence of these polymorphisms may indicate an increased risk of NMSC development in affected people.

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Silibinin and non-melanoma skin cancers.

Publications

Silibinin and non-melanoma skin cancers.

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