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Palmitoyl acyltransferase ZDHHC7 suppresses prostate cancer through inhibiting androgen receptor expression

ABSTRACT: Palmitoyl acyltransferase ZDHHC7 suppresses prostate cancer through inhibiting androgen receptor expression

PROVIDER: PRJNA922592 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23042800_1.fastq.gz	Fastqsanger.gz
	SRR23042800_2.fastq.gz	Fastqsanger.gz
	SRR23042801_1.fastq.gz	Fastqsanger.gz
	SRR23042801_2.fastq.gz	Fastqsanger.gz
	SRR23042802_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Palmitoyl acyltransferase ZDHHC7 suppresses prostate cancer through inhibiting androgen receptor expression

Project description:We examined ZDHHC family gene expression in human tissue collection and identified ZDHHC7 as a PCa-relevant member. RNA-seq analyses of PCa cells with ZDHHC7 de-regulation revealed global alterations in androgen response and cell cycle pathways. Mechanistically, ZDHHC7 inhibits AR gene transcription and therefore reduces AR protein levels and abolishes AR signaling in PCa cells. Accordingly, ZDHHC7 depletion increased oncogenic properties of PCa cells, whereas restoring ZDHHC7 is sufficient to suppress PCa cell proliferation and invasion in vitro and mitigate xenograft tumor growth in vivo. Lastly, we demonstrated that ZDHHC7 is down-regulated in human PCa compared to benign adjacent tissues and its loss is associated with worse clinical outcomes. Taken together, our findings unequivocally prove ZDHHC7 as a tumor suppressor gene that inhibits AR signaling and PCa progression, identifying ZDHHC7 loss as a biomarker for aggressive PCa and a target for therapeutic intervention.

2023-05-14 | GSE222592 | GEO

Deficiency of the palmitoyl acyltransferase ZDHHC7 modulates gene expression in mice after a mild chronic stress paradigm

Project description:Chronic stress (CS) is a debilitating condition that negatively affects body and brain. In mice, CS effects range from changes in behaviour down to the level of gene expression. These effects are partly mediated by sex and sex steroid hormones, which in turn are affected by the palmitoyl acyltransferase ZDHHC7. ZDHHC7 might modulate also the response to CS via palmitoylation of sex steroid hormone receptors and other proteins critical for neuronal structure and functions. Therefore, we aimed to investigate the role of ZDHHC7 in response to CS on different system levels in a mouse model of Zdhhc7-deficiency. Female and male Zdhhc7-knockout (KO) and -wildtype (WT) mice underwent a four-week-mild CS paradigm or non-stress control (C) condition. After C or CS, amongst other analyses, brain gene expression profiles (via mRNA-seq transcriptomics) were investigated. Analyses focused on effects of genotype (KO vs. WT) or condition (C vs. CS) separately in both sexes. Our results revealed significant effects particularly in females. Female KOs showed upregulated cortistatin expression after CS (C vs. CS: p<0.05). Zdhhc7-deficiency seemed to be related to a sex-specific stress response and may reveal genetic factors of CS-resilience in female mice.

2025-01-24 | GSE281404 | GEO

Deficiency of the palmitoyl acyltransferase ZDHHC7 modulates gene expression in mice after a mild chronic stress paradigm

Project description:Deficiency of the palmitoyl acyltransferase ZDHHC7 modulates gene expression in mice after a mild chronic stress paradigm

| PRJNA1183804 | ENA

KLF10 promotes nonalcoholic steatohepatitis progression through transcriptional activation of zDHHC7 [KFL10 overexpression]

Project description:Nonalcoholic steatohepatitis (NASH), characterized by hepatic steatosis, inflammation, and liver injury, has become a leading cause of end-stage liver diseases and liver transplantation. Krüppel-like factors 10 (KLF10) is a Cys2/His2 zinc finger transcription factor that regulates cell growth, apoptosis, and differentiation. However, whether it plays a role in the development and progression of chronic liver diseases like NASH remains poorly understood. In the present study, we found that KLF10 expression was selectively upregulated in the mouse models and human patients with NASH, compared with simple steatosis (NAFL). Gain- and loss-of function studies demonstrated that hepatocyte-specific overexpression of KLF10 aggravated, whereas its depletion alleviated diet-induced NASH pathogenesis in mice. Mechanistically, transcriptomic analysis and subsequent functional experiments showed that KLF10 promotes hepatic lipid accumulation and inflammation through the palmitoylation and plasma membrane localization of fatty acid translocase CD36 via transcriptionally activation of zDHHC7. Indeed, both expression of zDHHC7 and palmitoylation of CD36 are required for the pathogenic roles of KLF10 in NASH progression. Thus, our results identify an important role for KLF10 in NAFL-to-NASH development through zDHHC7-mediated CD36 palmitoylation.

2022-02-25 | GSE197054 | GEO

KLF10 promotes nonalcoholic steatohepatitis progression through transcriptional activation of zDHHC7 [NAFL vs NASH]

2022-02-25 | GSE197053 | GEO

DHHC7-mediated palmitoylation of barttin is a risk factor for Bartter syndrome

Project description:Chloride permeability in the thin and thick ascending limbs of the loop of Henle is a crucial component for urine concentration, with ClC-K/barttin chloride channels as a central component in establishing the cortico-medullary osmotic gradient. Barttin is an accessory subunit of human ClC-K channels, promoting trafficking of the ClC-K/barttin complex to the plasma membrane, increasing channel stability, and switching ClC-K/barttin channels into an active state. Barttin undergoes post-translational palmitoylation, which is essential for channel activation. Here, we identified DHHC7 as a major barttin palmitoyl-acyltransferase, the depletion of which reduced barttin palmitoylation and the macroscopic current amplitudes in cells expressing ClC-K/barttin channels. To investigate a functional role of barttin palmitoylation in vivo, we established Zdhhc7-/- mice. Although barttin palmitoylation was significantly decreased in the kidneys of Zdhhc7-/- animals, it did not result in any pathological consequences for kidney structure or function under physiological conditions. However, when Zdhhc7-/- animals were fed a low-salt diet, they developed hyponatremia and mild metabolic alkalosis, symptoms characteristic of human Bartter syndrome (BS) Type IV with mild progression. Notably, decreased barttin palmitoylation was also found for the R8L barttin mutant identified in human BS Type IV. These data suggest that barttin palmitoylation plays an important role in chloride channel dysfunction in certain variants of BS. Thus, our study provides evidence of the downregulation of barttin palmitoylation as a possible mechanism in the etiology of BS, making the restoration of barttin palmitoylation a promising clinical strategy for the treatment of Type IV BS.

2020-03-31 | PXD017231 | Pride

Inhibiting Monoacylglycerol Acyltransferase 1 Ameliorates Hepatic Metabolic Abnormalities, but not Inflammation and Injury in Mice

Project description:Abnormalities in hepatic lipid metabolism are believed to play a critical role in the etiology of nonalcoholic steatohepatitis (NASH). Monoacylglycerol acyltransferase (MGAT) enzymes convert monoacylglycerol to diacylglycerol, which is the penultimate step in one pathway for triacylglycerol (TAG) synthesis. Hepatic expression of Mogat1, which encodes an MGAT enzyme, is increased in the livers of mice with hepatic steatosis and knocking down Mogat1 improves insulin sensitivity, but whether increased MGAT activity plays a role in the etiology of NASH is unclear. To examine the effects of knocking down Mogat1 in the liver on the development of NASH, C57BL/6 mice were placed on a diet containing high levels of trans fatty acids, fructose, and cholesterol (HTF-C diet) or a low fat control diet for 4 weeks. Mice were then injected with antisense oligonucleotides (ASO) to knockdown Mogat1 or a scrambled ASO control for 12 weeks while remaining on diet. HTF-C diet caused glucose intolerance, hepatic steatosis, and induced hepatic gene expression markers of inflammation, macrophage infiltration, and stellate cell activation. Mogat1 ASO treatment, which suppressed Mogat1 expression in liver, attenuated weight gain, improved glucose tolerance, and decreased hepatic TAG content compared to control ASO-treated mice on HTF-C chow. However, Mogat1 ASO treatment did not reduce hepatic DAG, cholesterol, or free fatty acid content, improve histologic measures of liver injury, or reduce expression of markers of stellate cell activation, liver inflammation, and injury. In conclusion, inhibition of hepatic Mogat1 in HTF-C diet-fed mice improves glucose tolerance and hepatic TAG accumulation without attenuating liver inflammation and injury. Total RNA obtained from liver of 4 control vs. 4 Mogat1 ASO treated higf-fat diet (HFD) fed mice.

2014-11-05 | E-GEOD-60349 | biostudies-arrayexpress

acyltransferase brachypodium-arabidopsis-Impact of Brachypodium acyl-transferases

Project description:ra15-03_oxpmt7-7 - acyltransferase brachypodium-arabidopsis - What biochemical function? What consequence on lignification when overexpressed in Arabidopsis thaliana? - Transcripts of Arabidopsis stem overexpressing an acyl transferase from Brachypodium are compared to wild type plants. The overexpression is under a specific promoter (C4H).

2018-10-01 | GSE120114 | GEO

acyltransferase brachypodium-arabidopsis-Impact of Brachypodium acyl-transferases

Project description:acyltransferase brachypodium-arabidopsis-Impact of Brachypodium acyl-transferases

| PRJNA491727 | ENA

Inhibiting Androgen Receptor Splice Variants with Cysteine-Selective Irreversible Covalent Inhibitors to Treat Prostate Cancer

Project description:Inhibiting Androgen Receptor Splice Variants with Cysteine-Selective Irreversible Covalent Inhibitors to Treat Prostate Cancer

| PRJNA889781 | ENA

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