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Epidermal fatty acid binding protein prevents chemical-induced skin tumorigenesis by inhibition of SOX2 expression in keratinocytes

ABSTRACT: Epidermal fatty acid binding protein prevents chemical-induced skin tumorigenesis by inhibition of SOX2 expression in keratinocytes

PROVIDER: PRJNA431447 | ENA |

REPOSITORIES: ENA

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Epidermal fatty acid binding protein prevents chemical-induced skin tumorigenesis by inhibition of SOX2 expression in keratinocytes

Project description:E-FABP expression in keratinocytes increase interferons, in particualur IFNlamda, expression, which activate P53, a critical tumor suppessor, to inhibit or prevent chemical-induced skin tumorigenesis.

2018-08-30 | GSE109583 | GEO

cFLIP prevents TNFR1-dependent lethal dermatitis and TNFR1-independent blockade of epidermal differentiation

Project description:Cellular FLICE-inhibitory protein (cFLIP) prevents the development of dermatitis by blocking TNFα-dependent apoptosis of keratinocytes. However, it is unclear whether TNFα-independent signal might also contribute to the development of dermatitis in epidermis-specific Cflar-deficient (Cflar) mice. Here we show that Cflar;Tnfrsf1a-/- mice were born at the expected Mendelian ratio, but developed severe dermatitis and succumbed soon after birth. While keratinocytes still died by apoptosis, expression of epidermal differentiation markers, such as Loricrin, Filaggrin, and Keratin (Krt)10, but not Krt5 were severely downregulated in the skin of Cflar;Tnfrsf1a-/- mice at both mRNA and protein levels. Conversely, inflammatory cytokines, such as interleukin (IL)-6 and Il17a were elevated in the skin of Cflar ;Tnfrsf1a-/- mice. Treatment of primary keratinocytes with IL-6, to a lesser extent IL-17A suppressed expression of Loricrin, Filaggrin, and Krt10. Together, cFLIP suppresses TNFR1-independent apoptosis of keratinocytes and prevents IL-6-dependent blockade of epidermal differentiation.

2020-04-01 | GSE99379 | GEO

Epidermal FABP Prevents Chemical-Induced Skin Tumorigenesis by Regulation of TPA-Induced IFN/p53/SOX2 Pathway in Keratinocytes.

Project description:Skin lipids (e.g., fatty acids) are essential for normal skin functions. Epidermal FABP (E-FABP) is the predominant FABP expressed in skin epidermis. However, the role of E-FABP in skin homeostasis and pathology remains largely unknown. Herein, we utilized the 7,12-dimethylbenz(a)anthracene and 12-O-tetradecanolyphorbol-13-acetate-induced skin tumorigenesis model to assess the role of E-FABP in chemical-induced skin tumorigenesis. Compared to their wild-type littermates, mice deficient in E-FABP, but not adipose FABP, developed more skin tumors with higher incidence. 12-O-tetradecanolyphorbol-13-acetate functioning as a tumor promoter induced E-FABP expression and initiated extensive flaring inflammation in skin. Interestingly, 12-O-tetradecanolyphorbol-13-acetate -induced production of IFN-β and IFN-λ in the skin tissue was dependent on E-FABP expression. Further protein and gene expression arrays demonstrated that E-FABP was critical in enhancing IFN-induced p53 responses and in suppressing SOX2 expression in keratinocytes. Thus, E-FABP expression in skin suppresses chemical-induced skin tumorigenesis through regulation of IFN/p53/SOX2 pathway. Collectively, our data suggest an unknown function of E-FABP in prevention of skin tumor development, and offer E-FABP as a therapeutic target for improving skin innate immunity in chemical-induced skin tumor prevention.

| S-EPMC6109432 | biostudies-literature

Adenosine stimulation of normal human epidermal keratinocytes (NHEK)

Project description:Gene expression profile of normal human epidermal keratinocytes treated with adenosine

2021-01-22 | GSE165222 | GEO

Transcriptional targets of EphB2 and Ephrin-A4 signaling in epidermal keratinocytes

Project description:Human epidermal keratinocytes were treated with 25 ng.ml EphB2 or EFNA4, both as-Fc conjugates (Sigma). Human epidermal keratinocytes are treated with 25 ng/ml EphB2 or EFNA4 Fc conjugates in a 48hr time course.

2011-03-01 | E-GEOD-26523 | biostudies-arrayexpress

Human epidermal keratinocytes treated with retinoic acid or thyroid hormone

Project description:Targets of Retinoic Acid (RA) were identified in primary human epidermal keratinocytes grown in the presence or absence of all-trans retinoic acid for 1, 4, 24, 48 and 72 hours. Targets of Thyroid Hormone (T3) were identified in primary human epidermal keratinocytes grown in the presence or absence of the hormone; same controls as for RA.

2010-06-11 | GSE22298 | GEO

Human epidermal keratinocytes treated with retinoic acid or thyroid hormone

2010-06-23 | E-GEOD-22298 | biostudies-arrayexpress

Effects of leptin on gene transcription of human epidermal keratinocytes

Project description:Subcutaneous fat adipocytes and dermal adipocytes produce leptin. Association of leptin with cutaneous would healing is known, however, the response of human epidermal keratinocytes to leptin has not unclear in a molecular level. In order to get biological insights on the role of leptin in epidermal physiology, the genome scale transcriptional response of normal human keratinocytes to leptin was investigated.

2017-09-01 | GSE90979 | GEO

Epidermal differentiation: basal vs. suprabasal keratinocytes

Project description:In epidermal differentiation basal keratinocytes detach from the basement membrane, stop proliferating, and express a new set of structural proteins and enzymes, which results in an impermeable protein/lipid barrier that protects us. To define the transcriptional changes essential for this process, we purified large quantities of basal and suprabasal cells from human epidermis, using the expression of b4 integrin as the discriminating factor. The expected expression differences in cytoskeletal, cell cycle and adhesion genes confirmed the effective separation of the cell populations. Using DNA microarray chips, we comprehensively identify the differences in genes expressed in basal and differentiating layers of the epidermis, including the ECM components produced by the basal cells, the proteases in both the basal and suprabasal cells, and the lipid and steroid metabolism enzymes in suprabasal cells responsible for the permeability barrier. We identified the signaling pathways specific for the two populations, and found two previously unknown paracrine and one juxtacrine signaling pathway operating between the basal and suprabasal cells. Furthermore, using specific expression signatures, we identified a new set of late differentiation markers and mapped their chromosomal loci, as well as a new set of melanocyte-specific markers. The data represent a quantum jump in understanding the mechanisms of epidermal differentiation. Basal keratinocytes are defined as integrin b4-positive. Suprabasal sample contains all melanocytes as well. Basal (integrin b4+), suprabasal (b4-) and total epidermal keratinocytes. In duplicate, from 2 independent donors, breast reduction surgery.

2010-12-15 | E-GEOD-26059 | biostudies-arrayexpress

ROS stress responses of primary human epidermal keratinocytes

Project description:Primary human epidermal keratinocytes were exposed to in-vitro UVA-oxidized 1-palmitoyl-2-arachidonoyl-phosphatidylcholine or to UVA in presence and absence of a commercial UVA filter.

2018-11-28 | GSE104870 | GEO

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