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Novel Lipogenic Enzyme ELOVL7 Involves in Prostate Cancer Growth through Saturated Fatty-acid and Steroid Metabolism

ABSTRACT: We identified a novel lipogenic gene, ELOVL7, as an over-expressed gene in prostate cancer (PC) cells and it is involved in elongation of long-chain fatty acids and can play some important roles in prostate carcinogenesis. To investigate into downstream pathways of ELOVL7, we performed the gene expression analysis by the genome-wide cDNA microarrays. The genome–wide gene expression patterns were compared between PC cells transfected with siELOVL7 and these with siCONTROL and between the ELOVL7-overexpressing in-vivo tumors in mice bread with high fat diet (HFD) and those with normal diet (ND). HFD treatment significantly promoted the growth of ELOVL7-overexpressed PC cells in vivo. As a result, we identified five genes (IER3, HDAC8, GDF15, UGT2B11, and S1PR3) whose expressions were down-regulated with 20% and more in ELOVL7 knockdown and also were up-regulated with 20% and more in the tumors in the mice bread with HFD.

ORGANISM(S): Homo sapiens

PROVIDER: GSE14852 | GEO | 2009/04/01

SECONDARY ACCESSION(S): PRJNA112131

REPOSITORIES: GEO

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Novel Lipogenic Enzyme ELOVL7 Involves in Prostate Cancer Growth through Saturated Fatty-acid and Steroid Metabolism

Project description:We identified a novel lipogenic gene, ELOVL7, as an over-expressed gene in prostate cancer (PC) cells and it is involved in elongation of long-chain fatty acids and can play some important roles in prostate carcinogenesis. To investigate into downstream pathways of ELOVL7, we performed the gene expression analysis by the genome-wide cDNA microarrays. The genome–wide gene expression patterns were compared between PC cells transfected with siELOVL7 and these with siCONTROL and between the ELOVL7-overexpressing in-vivo tumors in mice bread with high fat diet (HFD) and those with normal diet (ND). HFD treatment significantly promoted the growth of ELOVL7-overexpressed PC cells in vivo. As a result, we identified five genes (IER3, HDAC8, GDF15, UGT2B11, and S1PR3) whose expressions were down-regulated with 20% and more in ELOVL7 knockdown and also were up-regulated with 20% and more in the tumors in the mice bread with HFD. The genome–wide gene expression patterns were compared between PC cells transfected with siELOVL7 and these with siCONTROL and between the ELOVL7-overexpressing in-vivo tumors bread with high fat diet (HFD) and those with normal diet (ND). HFD treatment significantly promoted the growth of ELOVL7-overexpressed PC cells in vivo.　The competitive hybridization was performed three times for each comparison (siELOVL7-1, -2, and-3; HFD-1, -2, and -3).

2009-04-01 | E-GEOD-14852 | biostudies-arrayexpress

High fat diet mice intestinal epithelial exosomal proteins were analyzed by MSMS.

Project description:High-fat diet (HFD) decreases insulin sensitivity. How high-fat diet causes insulin resistance is largely unknown. Here, we show that lean mice become insulin resistant after being administered exosomes isolated from the feces of obese mice fed a high-fat diet (HFD) or from human type II diabetic patients with diabetes. HFD altered the lipid composition of exosomes from predominantly PE in exosomes from lean animals (L-Exo) to PC in exosomes from obese animals (H-Exo). Mechanistically, we show that intestinal H-Exo is taken up by macrophages and hepatocytes, leading to inhibition of the insulin signaling pathway. Moreover, exosome-derived PC binds to and activates AhR, leading to inhibition of the expression of genes essential for activation of the insulin signaling pathway, including IRS-2, and its downstream genes PI3K and Akt. Together, our results reveal HFD-induced exosomes as potential contributors to the development of insulin resistance. Intestinal exosomes thus have potential as broad therapeutic targets.

2021-03-23 | PXD022641 | Pride

Identification of CD44 downstream target genes

Project description:CD44 expression has been shown to be enhanced in the liver and white adipose tissue (WAT) during obesity, suggesting a possible regulatory role for CD44 in metabolic syndrome. To study this hypothesis, we compared the gene expression profiles in liver and in WAT between WT and CD44 knockout (CD44KO) mice fed a high-fat diet (HFD) for 21 weeks. This analysis demonstrated that several genes associated with triglyceride synthesis and accumulation, including Mogat2, Cidea, Cidea, Apoa4, and Elovl7, were decreased in the livers of CD44KO mice compared to WT mice. Many genes encoding pro-inflammatory chemokines and chemokine receptors also were decreased in the livers of CD44KO mice. Analysis with WAT showed that genes associated with triglyceride accumulation, including Fasn, Elovl6 and Mogat2, were increased in WAT of CD44KO(HFD) mice compared to WT(HFD) mice. Moreover, many genes associated with inflammation, including cytokines (Cxcl14, Cxcl12, Il33, and Il2), cytokine receptors (Ccr1, Il6ra, Il10rb), trypases (Tpsb2, Tpsab1, Tpsg1), and cellular matrix proteins (Integrin ?4 (Itga4), ItgaM, Itgb2), were decreased in WAT of CD44(HFD) compared to WT(HFD) mice. This study indicates that CD44 plays a critical role in regulating several aspects of metabolic syndrome. Liver and white adipose tissue (WAT) total RNAs were purified from 5 WT and 5 CD44 knockout mice fed with a high-fat diet for 21 weeks. Then, samples were applied on Agilent mouse genome chips.

2013-06-01 | E-GEOD-43104 | biostudies-arrayexpress

Periprostatic fat gene expression in male mouse diet induced obesity and calorie restriction study

Project description:Obesity is associated with an increased incidence of high grade prostate cancer (PC) and worse prognosis for PC patients. Recently, we showed in men that obesity-related periprostatic white adipose tissue (WAT) inflammation, characterized by macrophages surrounding dead or dying adipocytes forming crown-like structures, was associated with high grade PC. Possibly, interventions that suppress periprostatic WAT inflammation will improve outcomes for men with PC. We found that supplemental 17β-estradiol (E2) could decrease periprostatic WAT inflammation in obese male mice in association with reduction in weight and calorie consumption. Here, we tested the hypothesis that calorie restriction alone would have similar effects on periprostatic WAT inflammation in obese male mice. To test this hypothesis, male mice were fed high fat diet to induce obesity and then switched to a 30% caloric restriction diet for an addition 7 weeks until sacrifice. LFD fed mice and mice fed HFD ad libitum serve as controls.

2019-07-22 | GSE123348 | GEO

Hsa-miR-1-2/miR-133a-1 cluster expression silencing by DNA hypermethylation triggers oncogenes contributing to prostate cancer aggressiveness

Project description:We developed a metabolic syndrome (MeS)-like disease model using C57BL/6J mice chronically fed with high fat diet (HFD) that were inoculated with TRAMP-C1 prostate cancer (PCa) cells to investigate the effect of a HFD on the expression of cancer-related miRNAs. In this dataset, we include the expression data obtained from TRAMP-C1 tumors developed in control diet (CD) versus high fat diet (HFD) C57BL/6J male mice. For differential expression analysis we used the Rank Product Method for two class unpaired data and a fold discovery rate (FDR) < 0.05 .

2022-11-16 | GSE181350 | GEO

Identification of CD44 downstream target genes

Project description:CD44 expression has been shown to be enhanced in the liver and white adipose tissue (WAT) during obesity, suggesting a possible regulatory role for CD44 in metabolic syndrome. To study this hypothesis, we compared the gene expression profiles in liver and in WAT between WT and CD44 knockout (CD44KO) mice fed a high-fat diet (HFD) for 21 weeks. This analysis demonstrated that several genes associated with triglyceride synthesis and accumulation, including Mogat2, Cidea, Cidea, Apoa4, and Elovl7, were decreased in the livers of CD44KO mice compared to WT mice. Many genes encoding pro-inflammatory chemokines and chemokine receptors also were decreased in the livers of CD44KO mice. Analysis with WAT showed that genes associated with triglyceride accumulation, including Fasn, Elovl6 and Mogat2, were increased in WAT of CD44KO(HFD) mice compared to WT(HFD) mice. Moreover, many genes associated with inflammation, including cytokines (Cxcl14, Cxcl12, Il33, and Il2), cytokine receptors (Ccr1, Il6ra, Il10rb), trypases (Tpsb2, Tpsab1, Tpsg1), and cellular matrix proteins (Integrin α4 (Itga4), ItgaM, Itgb2), were decreased in WAT of CD44(HFD) compared to WT(HFD) mice. This study indicates that CD44 plays a critical role in regulating several aspects of metabolic syndrome.

2013-06-01 | GSE43104 | GEO

Prostate cancer cells, Phosphorylation, LC-MS/MS

Project description:Prostate cancer is the second-leading cause of cancer deaths for men in the U.SS. Global phosphorylation study on prostate cancer is still rare, in this study SILAC and TiO2 were used to quantify the phosphorylation in PC-3 cell and PC-3M cell. Global proteomics analysis was used to comparative analysis the protein level in the PC-3 cell and PC-3M cell.

2020-07-22 | PXD016282 | Pride

High-fat diet fuels prostate cancer progression by rewiring the metabolome and amplifying the MYC program

Project description:Systemic metabolic alterations associated with increased consumption of saturated fat and obesity are linked with increased risk of prostate cancer progression and mortality but the molecular underpinnings of this association are poorly understood. Furthermore, the mechanisms by which metabolic rewiring alters the prostate cancer epigenome, the effector arm of intra- and extra-cellular signals, is equally nebulous. Here, we demonstrate, in a murine prostate cancer model, that high-fat diet (HFD) enhances the MYC transcriptional program through metabolic alterations that favour histone H4K20 hypomethylation at the promoter regions of MYC regulated genes, leading to a HFD-dependent phenotype characterized by increased cellular proliferation and tumour burden. Importantly, these results are recapitulated in prostate cancer patients, where increased saturated fat intake (SFI), but not monounsaturated or polyunsaturated fat intake, is also associated with an enhanced MYC transcriptional signature. Additionally, the SFI-induced MYC signature independently predicts prostate cancer progression and death. Finally, a dietary intervention consisting of switching from a high-fat to control diet, greatly attenuates the MYC transcriptional program. Our findings suggest that in primary prostate cancer, dietary saturated fat intake contributes to tumour progression by mimicking MYC over expression, setting the stage for therapeutic approaches involving changes to the diet.

2019-08-21 | GSE90910 | GEO

High-fat diet fuels prostate cancer progression by rewiring the metabolome and amplifying the MYC program

2019-08-21 | GSE90905 | GEO

High-fat diet fuels prostate cancer progression by rewiring the metabolome and amplifying the MYC program

Project description:Systemic metabolic alterations associated with increased consumption of saturated fat and obesity are linked with increased risk of prostate cancer progression and mortality, but the molecular underpinnings of this association are poorly understood. Here, we demonstrate in a murine prostate cancer model, that high-fat diet (HFD) enhances the MYC transcriptional program through metabolic alterations that favour histone H4K20 hypomethylation at the promoter regions of MYC regulated genes, leading to increased cellular proliferation and tumour burden. Saturated fat intake (SFI) is also associated with an enhanced MYC transcriptional signature in prostate cancer patients. The SFI-induced MYC signature independently predicts prostate cancer progression and death. Finally, switching from a high-fat to a low-fat diet, attenuates the MYC transcriptional program in mice. Our findings suggest that in primary prostate cancer, dietary SFI contributes to tumour progression by mimicking MYC over expression, setting the stage for therapeutic approaches involving changes to the diet.

2019-08-22 | MTBLS135 | MetaboLights

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