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Higher self renewal and oncogenic potential of keratinocytes from Black versus White populations linked to the hydroxysteroid dehydrogenase HSD17B7 gene [HSD17B7 overexpression]

ABSTRACT: Transcriptomic profiling of 3 human keratinocytes strains with HSD17B7 overexpression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE172288 | GEO | 2021/05/12

REPOSITORIES: GEO

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Higher self renewal and oncogenic potential of keratinocytes from Black versus White populations linked to the hydroxysteroid dehydrogenase HSD17B7 gene.

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Higher self renewal and oncogenic potential of keratinocytes from Black versus White populations linked to the hydroxysteroid dehydrogenase HSD17B7 gene

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Higher self renewal and oncogenic potential of keratinocytes from Black versus White populations linked to the hydroxysteroid dehydrogenase HSD17B7 gene [HSD17B7 overexpression]

Project description:Higher self renewal and oncogenic potential of keratinocytes from Black versus White populations linked to the hydroxysteroid dehydrogenase HSD17B7 gene [HSD17B7 overexpression]

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Higher self renewal and oncogenic potential of keratinocytes from Black versus White populations linked to the hydroxysteroid dehydrogenase HSD17B7 gene

Project description:Higher self renewal and oncogenic potential of keratinocytes from Black versus White populations linked to the hydroxysteroid dehydrogenase HSD17B7 gene

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Higher self renewal and oncogenic potential of keratinocytes from Black versus White populations linked to the hydroxysteroid dehydrogenase HSD17B7 gene.

Project description:Higher self renewal and oncogenic potential of keratinocytes from Black versus White populations linked to the hydroxysteroid dehydrogenase HSD17B7 gene.

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HSD17B7 gene in self-renewal and oncogenicity of keratinocytes from Black versus White populations

Project description:Human populations of Black African ancestry have a relatively high risk of aggressive cancer types, including keratinocyte-derived squamous cell carcinomas (SCCs). We show that primary keratinocytes (HKCs) from Black African (Black) versus White Caucasian (White) individuals have on average higher oncogenic and self-renewal potential, which are inversely related to mitochondrial electron transfer chain activity and ATP and ROS production. HSD17B7 is the top-ranked differentially expressed gene in HKCs and Head/Neck SCCs from individuals of Black African versus Caucasian ancestries, with several ancestry-specific eQTLs linked to its expression. Mirroring the differences between Black and White HKCs, modulation of the gene, coding for an enzyme involved in sex steroid and cholesterol biosynthesis, determines HKC and SCC cell proliferation and oncogenicity as well as mitochondrial OXPHOS activity. Overall, the findings point to a targetable determinant of cancer susceptibility among different human populations, amenable to prevention and management of the disease.

| S-SCDT-EMM-2021-14133 | biostudies-other

HSD17B7 gene in self-renewal and oncogenicity of keratinocytes from Black versus White populations.

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Conversion of mammalian 3alpha-hydroxysteroid dehydrogenase to 20alpha-hydroxysteroid dehydrogenase using loop chimeras: changing specificity from androgens to progestins.

Project description:Hydroxysteroid dehydrogenases (HSDs) regulate the occupancy and activation of steroid hormone receptors by converting potent steroid hormones into their cognate inactive metabolites. 3alpha-HSD catalyzes the inactivation of androgens in the prostate by converting 5alpha-dihydrotestosterone to 3alpha-androstanediol, where excess 5alpha-dihydrotestosterone is implicated in prostate disease. By contrast, 20alpha-HSD catalyzes the inactivation of progestins in the ovary and placenta by converting progesterone to 20alpha-hydroxyprogesterone, where progesterone is essential for maintaining pregnancy. Mammalian 3alpha-HSDs and 20alpha-HSDs belong to the aldo-keto reductase superfamily and share 67% amino acid sequence identity yet show positional and stereospecificity for the formation of secondary alcohols on opposite ends of steroid hormone substrates. The crystal structure of 3alpha-HSD indicates that the mature steroid binding pocket consists of 10 residues located on five loops, including loop A and the mobile loops B and C. 3alpha-HSD was converted to 20alpha-HSD by replacing these loops with those found in 20alpha-HSD. However, when pocket residues in 3alpha-HSD were mutated to those found in 20alpha-HSD altered specificity was not achieved. Replacement of loop A created a 17beta-HSD activity that was absent in either 3alpha- or 20alpha-HSD. Once loops A and C were replaced, the chimera had both 3alpha- and 20alpha-HSD activity. When loops A, B, and C were substituted, 3alpha-HSD was converted to a stereospecific 20alpha-HSD with a resultant shift in k(cat)/K(m) for the desired reaction of 2 x 10(11). This study represents an example where sex hormone specificity can be changed at the enzyme level.

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Dietary fatty acid composition alters 11β-hydroxysteroid dehydrogenase type 1 gene expression in rat retroperitoneal white adipose tissue.

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Central glucocorticoid administration promotes weight gain and increased 11β-hydroxysteroid dehydrogenase type 1 expression in white adipose tissue.

Project description:Glucocorticoids (GCs) are involved in multiple metabolic processes, including the regulation of insulin sensitivity and adipogenesis. Their action partly depends on their intracellular activation by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). We previously demonstrated that central GC administration promotes hyperphagia, body weight gain, hyperinsulinemia and marked insulin resistance at the level of skeletal muscles. Similar dysfunctions have been reported to occur upon specific overexpression of 11β-HSD1 in adipose tissue. The aim of the present study was therefore to determine whether the effects of central GC infusion may enhance local GC activation in white adipose tissue. Male Wistar and Sprague Dawley (SD) rats were intracerebroventricularly infused with GCs for 2 to 3 days. Body weight, food intake and metabolic parameters were measured, and expression of enzymes regulating 11β-HSD1, as well as that of genes regulated by GCs, were quantified. Central GC administration induced a significant increase in body weight gain and in 11β-HSD1 and resistin expression in adipose tissue. A decrease 11β-HSD1 expression was noticed in the liver of SD rats, as a partial compensatory mechanism. Such effects of GCs are centrally elicited. This model of icv dexamethasone infusion thus appears to be a valuable acute model, that helps delineating the initial metabolic defects occurring in obesity. An impaired downregulation of intracellular GC activation in adipose tissue may be important for the development of insulin resistance.

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