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Expression data of A939572 SCD1 inhibitor treated ccRCC cells

ABSTRACT: Presently, there is a deficiency of effective therapies designed to target clear cell renal cell carcinoma (ccRCC), with poor prognosis resulting in patients with advanced disease. Additionally, there is a lack of molecular factors which can be remedially targeted resulting in tumor specific inhibition, and therefore current therapeutic approaches often produce adverse side effects in patients. We identified that Stearoyl-CoA desaturase 1 (SCD1) was consistently overexpressed in patient ccRCC samples, and further investigation of SCD1 as a potential molecular target for ccRCC intervention utilizing a SCD1 inhibitor (A939572) resulted in tumor specific growth inhibition and induction of cell death. In order to understand the mechanism by which the SCD1 inhibitor mediated its anti-tumor effects, we performed gene array analysis and compared expression patterns between treated and untreated samples. Four established ccRCC cell lines purchased from ATCC were treated with DMSO control versus A939572 over a 24 hour time period. RNA from each group was isolated and sent of for gene array anaylsis. Gene expression data from each individual treatment group was normalized to its respective DMSO contol, and resulting expression patterns associated with drug exposure was compared between the four cell lines.

ORGANISM(S): Homo sapiens

SUBMITTER: Christina von Roemeling

PROVIDER: E-GEOD-41485 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data of A939572 SCD1 inhibitor treated ccRCC cells

Project description:Presently, there is a deficiency of effective therapies designed to target clear cell renal cell carcinoma (ccRCC), with poor prognosis resulting in patients with advanced disease. Additionally, there is a lack of molecular factors which can be remedially targeted resulting in tumor specific inhibition, and therefore current therapeutic approaches often produce adverse side effects in patients. We identified that Stearoyl-CoA desaturase 1 (SCD1) was consistently overexpressed in patient ccRCC samples, and further investigation of SCD1 as a potential molecular target for ccRCC intervention utilizing a SCD1 inhibitor (A939572) resulted in tumor specific growth inhibition and induction of cell death. In order to understand the mechanism by which the SCD1 inhibitor mediated its anti-tumor effects, we performed gene array analysis and compared expression patterns between treated and untreated samples.

2012-10-11 | GSE41485 | GEO

SCD1 Modulates the Skin Homeostasis via Sustaining Hemidesmosomes

Project description:Niche for stem cells can profoundly influence the position and fate of stem cells in tissue homeostasis and associated disorders, however, the mechanisms underlying the maintenance of stem cell niche remain poorly understood. Here we report that fatty acid desaturation catabolized by stearoyl-coenzyme A desaturase 1 (SCD1) regulates the activity of hair follicle stem cells (HFSCs) via blocking the formation of the bulge, a niche for HFSCs. We further unraveled that the abnormal hair growth in mice with SCD1 deletion is due to its function in K14+ basal keratinocytes rather than directly affecting HFSCs. Mechanistically, SCD1 deficiency impaired the expression of integrin α6 and the formation of hemidesmosomes (HDs), and thus allowed the activation of FAK in K14+ keratinocytes. Activated FAK subsequently stimulated PI3K and promoted the differentiation and proliferation of these keratinocytes, resulting in downward extension of the outer root sheath (ORS) and the disruption of bulge formation. Interestingly, inhibition of PI3K signaling restored bulge formation and normalized HFSCs and hair growth. Supplementation of oleic acid, the product of SCD1, to SCD1-/- mice also enhanced HD numbers, normalized the niche of HFSCs, and promoted hair growth in SCD1-/- mice. Taken together, SCD1 is indispensable for hair growth through stabilizing the number of HDs and thus sustaining bulge formation for HFSC residence and periodic activity.

2023-02-08 | GSE184346 | GEO

Transcriptomic analysis in airway epithelial cells in HDM-sensitized and SCD1 inhibitor-treated or vehicle-treated mice

Project description:Purpose: To elucidate the effects of SCD1 inhibitor in allergic airway inflammation. Method: Wild-type mice were sensitized intratracheally twice with house dust mite (HDM) extract at a 7-day interval. Along with that, an SCD-1 inhibitor, A939572 was also administered intraperitoneally daily. Airway epithelial cells were isolated by a cell sorter 48 h after the last senstization. N=2 each. Results: Using an optimized data analysis workflow, 385 transcripts showed differential expression between SCD1 inhibitor-treated mice and DMSO (vehicle)-treated mice with adjusted p value <0.05.

2022-04-01 | GSE190343 | GEO

Gene array analysis of clear cell renal cell carcinoma tissue versus matched normal kidney tissue

Project description:Currently there is a lack of effective therapies which result in long-term durable response for patients presenting with advanced and metastatic clear cell renal cell carcinoma (ccRCC). This is due in part to a lack of molecular factors which can be targeted pharmacologically. In order to identify novel tumor-specific targets, we performed high throughput gene array analysis screening numerous patient ccRCC tumor tissues across all stages of disease, and compared their gene expression levels to matched normal kidney. Our results identify a number of genes which demonstrate tumor-specific overexpression, and may present as novel targets for therapy. Patient tissue samples were sorted into disease stages based on pathology reports. RNA was extracted from flash frozen patient tumor and normal samples. Gene array analysis was performed, and resulting expression levels were compared between normal and tumor samples.

2014-01-03 | E-GEOD-53757 | biostudies-arrayexpress

Expression data in HCT-116 colon cancer cell treated with SCD1 inhibitor or in SCD1 knocked out HCT-116 cell

Project description:To understand molecular mechanisms underlying the growth inhibitory ativity of Stearoyl-CoA desaturase-1 (SCD1) inhibitor, we performed microarray analysis using HCT-116 colorectal cancer cells, in which SCD1 was pharmacologically blocked or genetically ablated.

2017-08-01 | GSE98364 | GEO

RNA sequencing analysis of wild-type and Scd1-deficient CD4+ naïve T cells

Project description:Analysis of differentially expressed genes in Scd1-deficient CD4+ naïve T cells. The goal of this study was to elucidate the underlying pathway of Scd1-deficiency leading to increased regulatory T cell differentiation.

2023-08-28 | GSE160040 | GEO

Regulation of the stress proteome by SCD1

Project description:Cytotoxic stress activates stress-activated kinases, initiates adaptive mechanisms, including the unfolded protein response (UPR) and autophagy, and induces programmed cell death. Fatty acid unsaturation prevents cytotoxic stress but the mechanisms are diffuse. We investigated changes in the proteome of NIH-3T3 fibroblasts upon induction of cytotoxic stress (valinomycin or myrtucommulone A) and SCD1 inhibition (CAY10566) and addressed the potential of PI(18:1/18:1) and PI(16:0/16:0) to compensate for the decrease in SCD1 activity.

2022-04-06 | PXD025396 | Pride

Scd1 Knockout Mice on very low fat diet

Project description:Stearoyl-CoA desaturase 1-deficient (SCD1-/-) mice have impaired monounsaturated fatty acid (MUFA) synthesis. When maintained on a very low-fat, high-carbohydrate (VLF-HC) diet, SCD1-/- mice develop severe hypercholesterolemia characterized by an increase in apolipoprotein B-containing lipoproteins and the appearance of lipoprotein-X. Additionally, high-density lipoprotein cholesterol is dramatically reduced in VLF-HC SCD1-/- mice. The concomitant presence of elevated plasma bile acids, bilirubin and aminotransferases in the VLF-HC SCD1-/- mouse are indicative of hepatic dysfunction. Supplementation of the VLF-HC diet with unsaturated fat (canola oil), but not saturated fat (coconut oil), prevents these plasma phenotypes. However, dietary oleate was not as effective as canola oil in reducing low-density lipoprotein cholesterol, signifying an additional role for dietary polyunsaturated fatty acid deficiency in the development of this phenotype. These results indicate that lack of SCD1 results in an increased requirement for dietary unsaturated fat to compensate for impaired MUFA synthesis and to prevent hypercholesterolemia and hepatic dysfunction. Keywords: repeat (genotype and diet)

2005-12-23 | GSE3889 | GEO

Escherichia coli SCD1

Project description:Escherichia coli SCD1 Genome sequencing and assembly

| PRJNA205120 | ENA

Expression data from Chinese renal cell carcinoma cells with FSTL1 knocked down

Project description:Clear cell renal cell carcinoma (ccRCC), the major histotype of cancer derived from kidney, is lack of robust prognostic and/or predictive biomarker and powerful therapeutic target. We previously identified that follistatin-like protein 1 (FSTL1) was significantly down-regulated in ccRCC at the transcription level. In the present study, we characterized, for the first time, that FSTL1 immunostaining was selectively positive in the cytoplasm of distal convoluted tubules. The expression of FSTL1 was significantly lower in ccRCC tissues than in adjacent renal tissues (P<0.001), as measured using immunohistochemistry in 69 patients with paired specimens, and lower in most ccRCC cell lines than in human embryonic kidney cells, as measured by quantitative RT-PCR. Multivariate Cox regression analysis in 89 patients with follow-up data showed that FSTL1 expression in tumors conferred a favorable postoperative prognosis independently, with a hazard ratio of 0.325 (95% confidence interval: 0.118-0.894). FSTL1 knockdown promoted anchorage independent growth, mobility, and invasion of ccRCC cell lines and promoted cell cycle from G0/G1 phases into S phase; while over-expression of FSTL1 significantly attenuated cell migration ability in ACHN cells. FSTL1 knockdown resulted in decreased expression of E-cadherin and increased expression of N-cadherin in ccRCC cell lines significantly, indicating that FSTL1 may attenuate epithelial to mesenchymal transition in ccRCC. Microarray assay indicated that NF-ÎºB and HIF-2Î± pathways were activated following FSTL1 knockdown in ccRCC cells. Our study indicates that FSTL1 serves as a tumor suppressor in ccRCC, up-regulation of FSTL1 in cancer cells may be a candidate target therapy for advanced ccRCC. RNA samples were collected from NRCC-shsiscramble, NRCC-shFSTL1-1 and NRCC-shFSTL1-2 cells. Then samples were hybridized to Affymetrix arrays for mRNA profiling.

2016-01-20 | E-GEOD-76948 | biostudies-arrayexpress

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