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ELOVL2 is a novel tumor suppressor attenuating tamoxifen resistance in breast cancer via suppressing the AKT pathway [methylation 450K]

ABSTRACT: ELOVL2 is a novel tumor suppressor attenuating tamoxifen resistance in breast cancer via suppressing the AKT pathway [methylation 450K]

PROVIDER: PRJNA548633 | ENA |

REPOSITORIES: ENA

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ELOVL2 is a novel tumor suppressor attenuating tamoxifen resistance in breast cancer via suppressing the AKT pathway [gene expression]

Project description:Analysis of tamoxifen-sensitivity recovery effect by genes which are regulated by ELOVL2(Elongation of very long chain fatty acids protein 2) at gene expression level in breast cancer. This study identifies that ELOVL2 regulates AKT or ER signaling-related genes and ELOVL2 as an essential gene responsible for resistance.

2020-06-12 | GSE132614 | GEO

ELOVL2 is a novel tumor suppressor attenuating tamoxifen resistance in breast cancer via suppressing the AKT pathway [methylation 450K]

Project description:Genome wide DNA methylation profiling of tamoxifen-resistant(Tam-R) breast cancer cell line MCF-7. The Illumina Infinium Human Methylation 450k Bead chip was used to obtain DNA methylation profiles across approximately 450,000 CpGs.

2020-06-12 | GSE132615 | GEO

ELOVL2 is a novel tumor suppressor attenuating tamoxifen resistance in breast cancer via suppressing the AKT pathway

Project description:ELOVL2 is a novel tumor suppressor attenuating tamoxifen resistance in breast cancer via suppressing the AKT pathway

| PRJNA548537 | ENA

ELOVL2 is a novel tumor suppressor attenuating tamoxifen resistance in breast cancer via suppressing the AKT pathway [methylation 850K]

Project description:ELOVL2 is a novel tumor suppressor attenuating tamoxifen resistance in breast cancer via suppressing the AKT pathway [methylation 850K]

| PRJNA548634 | ENA

ELOVL2 is a novel tumor suppressor attenuating tamoxifen resistance in breast cancer via suppressing the AKT pathway [gene expression]

Project description:ELOVL2 is a novel tumor suppressor attenuating tamoxifen resistance in breast cancer via suppressing the AKT pathway [gene expression]

| PRJNA548639 | ENA

ELOVL2 is a novel tumor suppressor attenuating tamoxifen resistance in breast cancer via suppressing the AKT pathway [methylation 850K]

Project description:Genome wide DNA methylation profiling of tamoxifen-resistant(Tam-R) breast cancer cell line MCF-7. The Illumina Infinium MethylationEPIC BeadChip was used to obtain DNA methylation profiles across approximately 850,000 CpGs.

2020-06-12 | GSE132616 | GEO

ELOVL2: a novel tumor suppressor attenuating tamoxifen resistance in breast cancer.

Project description:Epigenetic events have successfully explained the cause of various cancer types, but little is known about tamoxifen resistance (TamR) that induces cancer recurrence. In this study, via genome-wide methylation analysis in MCF-7/TamR cells we show that elongation of very-long chain fatty acid protein 2 (ELOVL2) was hypermethylated and downregulated in the samples from TamR breast cancer patients (n = 28) compared with those from Tam-sensitive (TamS) patients (n = 33) (P < 0.001). Strikingly, in addition to having tumor suppressor activity, ELOVL2 was shown to recover Tam sensitivity up to 70% in the MCF-7/TamR cells and in a xenograft mouse model. A group of genes in the AKT and ERa signaling pathways, e.g., THEM4, which play crucial roles in drug resistance, were found to be regulated by ELOVL2. This study implies that the deregulation of a gene in fatty acid metabolism can lead to drug resistance, giving insight into the development of a new therapeutic strategy for drug-resistant breast cancer.

| S-EPMC8263635 | biostudies-literature

ELOVL2 is a novel tumor suppressor attenuating tamoxifen resistance in breast cancer via suppressing the AKT pathway

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-06-12 | GSE132617 | GEO

RNAseq of Salmo salar parrs with CRISPR/Cas9 induced knockout in the elovl2 gene versus wild type

Project description:Atlantic salmon can synthesize polyunsaturated fatty acids (PUFAs), such as eicosapentaenoic acid (20:5n-3), arachidonic acid (20:4n-6) and docosahexaenoic acid (22:6n-3) via activities of very long chain fatty acyl elongases (elovls) and fatty acyl desaturases (fads), albeit to a limited degree. Understanding molecular mechanisms of PUFA biosynthesis and regulation is a pre-requisite for sustainable use of vegetable oils in aquafeeds as current sources of fish oils are unable to meet increasing demands for omega-3 PUFAs. By generating CRISPR-mediated elovl2 knockout, we have shown that elovl2 is crucial for multi-tissue synthesis of 22:6n-3 in vivo and endogenously synthesized PUFAs are important for transcriptional regulation of lipogenic genes in Atlantic salmon. The elovl2 knockouts showed reduced levels of 22:6n-3 and accumulation of 20:5n-3 and docosapentaenoic acid (22:5n-3) in the liver, brain and white muscle, suggesting inhibition of elongation. Additionally, elovl2-knockout salmon showed accumulation of 20:4n-6 in the brain and white muscle. The impaired synthesis of 22:6n-3 induced hepatic expression of sterol regulatory element binding protein-1 (srebp-1), fatty acid synthase-b, Δ6fad-a, Δ5fad and elovl5. Our study demonstrates key roles of elovl2 at two penultimate steps of PUFA synthesis in vivo and suggests Srebp-1 as a main regulator of PUFA synthesis in Atlantic salmon.

2019-04-30 | E-MTAB-7220 | biostudies-arrayexpress

Molecular phenotyping of multiple mouse strains under metabolic challenge uncovers Elovl2 as a novel regulator of glucose-induced insulin secretion

Project description:Defective insulin secretion by pancreatic Î² cells underlies the development of type 2 diabetes (T2D). High fat diet-fed mice are commonly used to study diabetes progression, but studies are usually limited to a single strain, such as C57Bl/6J. Here, we use a systems biology approach to integrate large phenotypic and islet transcriptomic data sets from six commonly used strains fed a high fat or regular chow diet to identify genes associated with glucose intolerance and insulin secretion. One of these genes is Elovl2, encoding very long chain fatty acid elongase 2. ELOVL2 is responsible for the synthesis of the polyunsaturated fatty acid, docosahexaenoic acid (DHA). We show that DHA rescues glucose-induced insulin secretion and cytosolic Ca2+ influx impaired by glucolipotoxicity, and that Elovl2 over-expression is able to restore the insulin secretion defect under these conditions. We propose that increased endogenous DHA levels resulting from Elovl2 up-regulation counteracts the insulin secretion defect associated with glucolipotoxicity. Although we focus our experimental validation on Elovl2, the comprehensive data set and integrative network model we used to identify this candidate gene represents an important novel resource to dissect the molecular aetiology of Î² cell failure in murine models. 6 mouse strains, 4 time points, 2 diets

2017-04-28 | E-GEOD-78183 | biostudies-arrayexpress

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