Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

β-Caryophyllene Enhances the Transcriptional Upregulation of SREBP-dependent Lipid Biosynthesis in Breast Cancer Cells

ABSTRACT: β-caryophyllene (BCP) exhibits anti-proliferative properties in cancer cells. Here, we examine the hypothesis that BCP induces membrane remodeling. Our data show that high concentrations of BCP increase membrane permeability of human breast cells (hBrC) causing detachment and cell death. At a “sub-lethal” concentration of BCP, we show that BCP induces a striking upregulation of genes involved in cholesterol biosynthesis, including the gene that encodes for HMGCoA reductase (HMGCR), the rate-determining step in cholesterol biosynthesis. In addition, stearoyl-CoA desaturase (SCD) is also upregulated which would lead to the enhanced formation of monounsaturated fatty acids, specifically oleate and palmitoleate from stearoyl CoA and palmitoyl CoA, respectively. These fatty acids are major components of membrane phospholipids and cholesterol esters. Together, these data suggest that cells respond to BCP by increasing the synthesis of components found in membranes. These responses could be viewed as a repair mechanism and/or as a mechanism to mount resistance to the cytotoxic effect of BCP. Blocking HMGCR enhances the cytotoxicity of BCP, suggesting that this may provide an additional therapeutic tool in controlling breast cancer cell growth, assuming that targeted specificity could be established.

ORGANISM(S): Homo sapiens

PROVIDER: GSE125511 | GEO | 2019/12/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Expression data from differentiated 3T3-L1 pre-adipocytes.

2014-04-04 | GSE51905 | GEO

Expression data from differentiated 3T3-L1 pre-adipocytes.

Project description:Stearoyl-CoA desaturase (SCD) is the rate-limiting enzyme catalyzing the conversion of saturated fatty acids palmitate and stearate to monounsaturated fatty acids palmitoleate and oleate. During adipocyte differentiation, SCD expression increases concomitantly with several transcription factors and lipogenic genes. We used microarrays to examine gene expression in differentiated pre-adipocytes treated with and without an SCD inhibitor. On day 7 of adipocyte differentiation, total RNA was extracted from adipocytes. Two conditions were selected for comparison: total RNA extracted from adipocytes treated with DMSO (control) and or a SCD inhibitor.

2014-04-04 | E-GEOD-51905 | biostudies-arrayexpress

Gene Expression Profiles of Scd1 knockout mice vs wild type mice on chow diet: Liver.

Project description:Loss of stearoyl-CoA desaturase-1 function protects mice against adiposity. Ntambi JM, Miyazaki M, Stoehr JP, Lan H, Kendziorski CM, Yandell BS, Song Y, Cohen P, Friedman JM, Attie AD. Department of Biochemistry, University of Wisconsin, Madison, WI 53706, USA. ntambi@biochem.wisc.edu Stearoyl-CoA desaturase (SCD) is a central lipogenic enzyme catalyzing the synthesis of monounsaturated fatty acids, mainly oleate (C18:1) and palmitoleate (C16:1), which are components of membrane phospholipids, triglycerides, wax esters, and cholesterol esters. Several SCD isoforms (SCD1-3) exist in the mouse. Here we show that mice with a targeted disruption of the SCD1 isoform have reduced body adiposity, increased insulin sensitivity, and are resistant to diet-induced weight gain. The protection from obesity involves increased energy expenditure and increased oxygen consumption. Compared with the wild-type mice the SCD1-/- mice have increased levels of plasma ketone bodies but reduced levels of plasma insulin and leptin. In the SCD1-/- mice, the expression of several genes of lipid oxidation are up-regulated, whereas lipid synthesis genes are down-regulated. These observations suggest that a consequence of SCD1 deficiency is an activation of lipid oxidation in addition to reduced triglyceride synthesis and storage. Keywords: Genetic modifications

2005-07-14 | GSE2926 | GEO

Stearoyl-CoA desaturase mediated monounsaturated fatty acid availability supports humoral immunity

Project description:Immune cells can metabolize fatty acids (FAs) to generate energy. The source of different fatty acid species, and their impacts on humoral immunity remains poorly understood. Here we report that proliferating B cells require increased amount of monounsaturated fatty acids (MUFA) to maintain mitochondrial metabolism and mTOR activity, and to prevent excessive autophagy and endoplasmic reticular (ER) stress. Furthermore, B cell extrinsic Stearoyl-Coa desaturase (SCD) activity generates endogenous MUFA to support early B cell development and germinal center (GC) formation in vivo during immunization and influenza infection. Thus, SCD-mediated MUFA production is critical for humoral immunity.

2020-12-02 | GSE162460 | GEO

Expression data from endothelial cells induced from bone marrow mesenchymal stem cells with SCD1 overexpression

Project description:Bone marrow mesenchymal stem cells (BM-MSCs) are of multi-differentiating potential and has been demonstrated to have the ability to differentiate into endothelial cells. Stearoyl-CoA desaturase 1 (SCD1) is a key enzyme in lipid metabolism, which can convert saturated fatty acids into unsaturated fatty acids. We used lentivirus to transfected SCD1 gene into BM-MSCs and found that overexpression of SCD1 could promote the differentiation of BM-MSCs into endothelial cells. We used microarrays to detect the differential gene expression profile of endothelial induced BM-MSCs with SCD1 overexpression.

2017-11-07 | GSE106596 | GEO

Transcription profiling of livers from SCD1 knockout and wild type mice to elucidate the molecular basis of protection against adiposity in mice lacking of stearoyl-CoA desaturase-1 function

Project description:Stearoyl-CoA desaturase (SCD) is a central lipogenic enzyme catalyzing the synthesis of monounsaturated fatty acids, mainly oleate (C18:1) and palmitoleate (C16:1), which are components of membrane phospholipids, triglycerides, wax esters, and cholesterol esters. Several SCD isoforms (SCD1-3) exist in the mouse. Here we show that mice with a targeted disruption of the SCD1 isoform have reduced body adiposity, increased insulin sensitivity, and are resistant to diet-induced weight gain. The protection from obesity involves increased energy expenditure and increased oxygen consumption. Compared with the wild-type mice the SCD1-/- mice have increased levels of plasma ketone bodies but reduced levels of plasma insulin and leptin. In the SCD1-/- mice, the expression of several genes of lipid oxidation are up-regulated, whereas lipid synthesis genes are down-regulated. These observations suggest that a consequence of SCD1 deficiency is an activation of lipid oxidation in addition to reduced triglyceride synthesis and storage. Experiment Overall Design: RNA was isolated from livers of 10 individual 6-week-old female mice by using a standard method. Mouse genome U74A arrays were used to monitor the expression level of approximately 10,000 genes and expressed sequence tags (Affymetrix). Genes differentially expressed were identified by comparing expression levels in SCD1-/- and wild-type mice.

2007-08-31 | E-GEOD-2926 | biostudies-arrayexpress

Transcription profiling of livers of stearoyl-CoA desaturase 1-deficient mice to search for gene expression changes unique to SCD1-/- mice on a very low-fat, high- carbohydrate 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. Experiment Overall Design: We used Affymetrix Mouse430v2.0 microarray chips to search for gene expression changes unique to the VLF-HC SCD1-/- group. These chips contain 45,101 probe sets representing over 39,000 transcripts and variants from over 34,000 mouse genes. We studied SCD1+/+ and SCD1-/- mice on chow or the VLF-HC diet, analyzing five individual livers from each subgroup for a total of twenty microarrays.

2007-11-01 | E-GEOD-3889 | biostudies-arrayexpress

The transcriptomic changes induced by NREP downregulation in HepG2 cells

Project description:To evaluate the global transcriptomic changes induced by Neuronal Regeneration Related Protein (NREP) downregulation, we employed RNA-sequencing in HepG2 cells lacking NREP. Enriched pathway analyses of upregulated genes revealed pathways involved in cholesterol synthesis, fatty acid metabolism, NAFLD and PI3K-250 AKT signaling. In contrast, enriched downregulated genes included those for membrane trafficking, non-sense mediated decay, glucagon signaling, and cell-cycle. Differentially expressed genes included HMGCR (cholesterol synthesis) and TGFBR1 (TGF-β signaling and fibrosis).

2021-01-04 | GSE141078 | GEO

Scd1 Knockout Mice on very low fat diet

2005-12-23 | GSE3889 | GEO

Expression data from human pluripotent stem cells and differentiated cells treated with pluripotent-specific inhibitors

Project description:The use of human pluripotent stem cells (hPSCs) in cell therapy is hindered by the tumorigenic risk from residual undifferentiated cells. Here we performed a high-throughput screen of over 52,000 small molecules, and identified 15 highly selective cytotoxic inhibitors of hPSCs (PluriSIns). Cellular and molecular analyses revealed that the most selective compound, PluriSIn #1, is a pluripotent-specific inhibitor of stearoyl-coA desaturase (SCD1), the key enzyme in the biosynthesis of monounsaturated fatty acids (MUFA). SCD1 inhibition in hPSCs induced ER stress, protein synthesis attenuation, and apoptosis of these cells, revealing that MUFA biosynthesis is crucial for their survival. PluriSIn #1 was also cytotoxic toward the ICM cells of mouse embryos, indicating that the dependence on SCD1 is inherent to the pluripotent state. Finally, application of PluriSIn #1 prevented teratoma formation from tumorigenic undifferentiated cells. Our novel method to eliminate undifferentiated cells from culture should thus increase the safety of hPSC-based treatments. Expression data from undifferentiated and differentiated human embryonic stem cells. Total RNA was isolated from undifferentiated human pluripotent stem cells grown on matrigel with mTeSR1 medium, or from early endodermal progenitor cells differentiated from human embryonic stem cells.

2013-01-22 | E-GEOD-37040 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data