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UVB drives transcriptomic and epigenetic reprogramming which can be protected by antioxidant sulforaphane in human skin keratinocytes

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE185321 | GEO | 2021/10/07

REPOSITORIES: GEO

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UVB drives transcriptomic and epigenetic reprogramming which can be protected by antioxidant sulforaphane in human skin keratinocytes [RNA-seq]

Project description:Continuous exposure to ultraviolet (UV) is one of the main factors contributing to skin carcinogenesis. Sulforaphane (SFN) is a potent antioxidative agent which has potential to prevent the UV-induced skin cell transformation. We characterized the transcriptome and CpG methylation profile of human keratinocytes (HaCaT cells) treated with UVB and/or SFN using RNA sequencing.

2021-10-07 | GSE185320 | GEO

UVB drives transcriptomic and epigenetic reprogramming which can be protected by antioxidant sulforaphane in human skin keratinocytes [Methyl-seq]

2021-10-07 | GSE185319 | GEO

UVB drives transcriptomic and epigenetic reprogramming which can be protected by antioxidant sulforaphane in human skin keratinocytes

Project description:UVB drives transcriptomic and epigenetic reprogramming which can be protected by antioxidant sulforaphane in human skin keratinocytes

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UVB drives transcriptomic and epigenetic reprogramming which can be protected by antioxidant sulforaphane in human skin keratinocytes [RNA-seq]

Project description:UVB drives transcriptomic and epigenetic reprogramming which can be protected by antioxidant sulforaphane in human skin keratinocytes [RNA-seq]

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UVB drives transcriptomic and epigenetic reprogramming which can be protected by antioxidant sulforaphane in human skin keratinocytes [Methyl-seq]

Project description:UVB drives transcriptomic and epigenetic reprogramming which can be protected by antioxidant sulforaphane in human skin keratinocytes [Methyl-seq]

| PRJNA768675 | ENA

Reprogramming of keratin biosynthesis by sulforaphane restores skin integrity in epidermolysis bullosa simplex.

Project description:Epidermolysis bullosa simplex (EBS) is a rare inherited condition in which the epidermis loses its integrity after mechanical trauma. EBS is typified by the dysfunction of intermediate filaments in basal keratinocytes of epidermis. Most cases of EBS are due to mutations in the keratin 5 or 14 gene (K5 and K14), whose products copolymerize to form intermediate filaments in basal keratinocytes. Available treatments for this disorder are only palliative. Here we exploit functional redundancy within the keratin gene family as the basis for therapy. We show that genetic activation of Gli2 or treatment with a pharmacological activator of Nrf2, two transcription factors eliciting distinct transcriptional programs, alleviates the blistering caused by a K14 deficiency in an EBS mouse model, correlating with K17 induction in basal epidermal keratinocytes. Nrf2 induction is brought about by treatment with sulforaphane, a natural product. Sulforaphane thus represents an attractive option for the prevention of skin blistering associated with K14 mutations in EBS.

| S-EPMC1964870 | biostudies-other

Pannexin 2 is expressed in murine skin and promotes UVB-induced apoptosis of keratinocytes.

Project description:Pannexins (PANX) are a family of three channel-forming membrane glycoproteins expressed in the skin. Previous studies have focused on the role of PANX1 and PANX3 in the regulation of cellular functions in skin cells while PANX2, the largest member of this protein family, has not been investigated. In the current study, we explored the temporal PANX2 expression in murine skin and found that one Panx2 splice variant (Panx2-202) tends to be more abundant at the protein level and is continuously expressed in developed skin. PANX2 was detected in the suprabasal layers of the mouse epidermis and up-regulated in an in vitro model of rat epidermal keratinocyte differentiation. Furthermore, we show that in apoptotic rat keratinocytes, upon UV light B (UVB)-induced caspase-3/7 activation, ectopically overexpressed PANX2 is cleaved in its C-terminal domain at the D416 residue without increasing the apoptotic rate measured by caspase-3/7 activation. Notably, CRISPR-Cas9 mediated genetic deletion of rat Panx2 delays but does not impair caspase-3/7 activation and cytotoxicity in UVB-irradiated keratinocytes. We propose that endogenous PANX2 expression in keratinocytes promotes cell death after UVB insult and may contribute to skin homeostasis.

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UVB drives different stages of epigenome alterations during progression of skin cancer.

Project description:Exposure to ultraviolet B (UVB) irradiation results in multitude of cellular responses including generation of reactive oxygen species and DNA damage and is responsible for non-melanoma skin cancers (NMSCs). Although genetic mutation is well documented, the epi-mutation, the alteration in epigenetics, remains elusive. In this study, we utilized CpG Methyl-seq to identify a genome-wide DNA CpG methylation, to profile the DNA methylation in UVB-irradiated SKH-1 mouse skin epidermis and non-melanoma skin papillomas at various stages. Methyl-seq and RNA-seq were performed to examine the methylation and corresponding transcriptome alterations. The methylation profiles in mouse epidermis were altered by UVB-irradiation as time progresses. Ingenuity Pathways Analysis (IPA) identified many cancer related pathways including PTEN, p53, Nrf2 and inflammatory signaling in UVB-irradiation induced carcinogenesis. Additionally, some novel genes involved in skin carcinogenesis that were not previously reported were differentially methylated, including Enf2, Mgst2, Vegfa, and Cdk4. Taken together, the current study provides novel profiles and insights of methylation and transcriptomic changes at different stages of carcinogenesis in UVB-irradiation induced NMSC and offers potential targets for prevention and treatment of NMSC at different stages of human skin cancer.

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Loss of tumor suppressor IGFBP4 drives epigenetic reprogramming in hepatic carcinogenesis.

Project description:Genomic sequencing of hepatocellular carcinoma (HCC) uncovers a paucity of actionable mutations, underscoring the necessity to exploit epigenetic vulnerabilities for therapeutics. In HCC, EZH2-mediated H3K27me3 represents a major oncogenic chromatin modification, but how it modulates the therapeutic vulnerability of signaling pathways remains unknown. Here, we show EZH2 acts antagonistically to AKT signaling in maintaining H3K27 methylome through epigenetic silencing of IGFBP4. ChIP-seq revealed enrichment of Ezh2/H3K27me3 at silenced loci in HBx-transgenic mouse-derived HCCs, including Igfbp4 whose down-regulation significantly correlated with EZH2 overexpression and poor survivals of HCC patients. Functional characterizations demonstrated potent growth- and invasion-suppressive functions of IGFBP4, which was associated with transcriptomic alterations leading to deregulation of multiple signaling pathways. Mechanistically, IGFBP4 stimulated AKT/EZH2 phosphorylation to abrogate H3K27me3-mediated silencing, forming a reciprocal feedback loop that suppressed core transcription factor networks (FOXA1/HNF1A/HNF4A/KLF9/NR1H4) for normal liver homeostasis. Consequently, the in vivo tumorigenicity of IGFBP4-silenced HCC cells was vulnerable to pharmacological inhibition of EZH2, but not AKT. Our study unveils chromatin regulation of a novel liver tumor suppressor IGFBP4, which constitutes an AKT-EZH2 reciprocal loop in driving H3K27me3-mediated epigenetic reprogramming. Defining the aberrant chromatin landscape of HCC sheds light into the mechanistic basis of effective EZH2-targeted inhibition.

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Metabolic Reprogramming Drives Pituitary Tumor Growth through Epigenetic Regulation of TERT.

Project description:Pituitary adenomas are common, benign brain tumors. Some tumors show aggressive phenotypes including early recurrence, local invasion and distant metastasis, but the underlying mechanism to drive the progression of pituitary tumors has remained to be clarified. Aerobic glycolysis known as the Warburg effect is one of the emerging hallmarks of cancer, which has an impact on the tumor biology partly through epigenetic regulation of the tumor-promoting genes. Here, we demonstrate metabolic reprogramming in pituitary tumors contributes to tumor cell growth with epigenetic changes such as histone acetylation. Notably, a shift in histone acetylation increases the expression of telomerase reverse transcriptase (TERT) oncogene, which drives metabolism-dependent cell proliferation in pituitary tumors. These indicate that epigenetic changes could be the specific biomarker for predicting the behavior of pituitary tumors and exploitable as a novel target for the aggressive types of the pituitary tumors.

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