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E-GEOD-22336

ABSTRACT: UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is an inducer of apoptotic processes in Capan-1 pancreatic carcinoma cells: GNE silencing

OTHER RELATED OMICS DATASETS IN: PRJNA129243PRJNA129245PRJNA127511

PROVIDER: E-GEOD-22336 | ExpressionAtlas | 2015-08-12

REPOSITORIES: ExpressionAtlas

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UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is an inducer of apoptotic processes in Capan-1 pancreatic carcinoma cells

Project description:This SuperSeries is composed of the following subset Series: GSE22334: Induction of apoptotic processes in Capan-1 pancreatic carcinoma cells by restoration of p16INK4a expression GSE22336: UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is an inducer of apoptotic processes in Capan-1 pancreatic carcinoma cells: GNE silencing Refer to individual Series

2010-08-01 | E-GEOD-22337 | biostudies-arrayexpress

Homo sapiens

Project description:UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is an inducer of apoptotic processes in Capan-1 pancreatic carcinoma cells: GNE silencing

| PRJNA129245 | ENA

Project description:UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is an inducer of apoptotic processes in Capan-1 pancreatic carcinoma cells

| PRJNA127511 | ENA

Homo sapiens

Project description:Induction of apoptotic processes in Capan-1 pancreatic carcinoma cells by restoration of p16INK4a expression

| PRJNA129243 | ENA

E-GEOD-22334

Project description:Induction of apoptotic processes in Capan-1 pancreatic carcinoma cells by restoration of p16INK4a expression

2015-08-12 | E-GEOD-22334 | ExpressionAtlas

EMT alterations in the solute carrier landscape uncover SLC22A10/A15 imposed vulnerabilities in pancreatic cancer

Project description:<p>The involvement of membrane-bound solute carriers (SLCs) in neoplastic transdifferentiation processes is poorly defined. Here, we examined changes in the SLC landscape during epithelial-mesenchymal transition (EMT) of pancreatic cancer cells. We show that two SLCs from the organic anion/cation transporter family, SLC22A10 and SLC22A15, favor EMT via interferon (IFN) α and γ signaling activation of receptor tyrosine kinase-like orphan receptor 1 (ROR1) expression. In addition, SLC22A10 and SLC22A15 allow tumor cell accumulation of glutathione to support EMT via the IFNα/γ-ROR1 axis. Moreover, a pan-SLC22A inhibitor lesinurad reduces EMT-induced metastasis and gemcitabine chemoresistance to prolong survival in mouse models of pancreatic cancer, thus identifying new vulnerabilities for human PDAC.</p>

2021-10-15 | MTBLS1925 | MetaboLights

Open chromatin in human pancreatic islets (FAIRE-seq) - Appendix to E-GEOD-17616

Project description:An appendix to the published Gaulton et al. work (PMID: 20118932; E-GEOD-17616). In the original paper, the authors note that samples 1 and 2 are not as pure as the third sample. This appendix provides FAIRE-Seq data obtained from a purified islet sample to replace the problematic published data. The goal of the original experiment was to identify active regulatory DNA in human pancreatic islets. This was accomplished using high-throughput sequencing of genomic regions isolated using FAIRE from three purified pancreatic islet samples to identify sites of open chromatin.

2014-12-23 | E-MTAB-3199 | biostudies-arrayexpress

Effects of AKT inhibition in the pancreatic cancer cell proteome

Project description:The AKT pathway is a major regulator of human pancreatic adenocarcinoma progression and a key pharmacological target. The mechanisms of adaptation to long-term silencing of AKT isoforms of human and mouse pancreatic adenocarcinoma cancer cells were studied.

2021-09-09 | PXD020673 | Pride

Project description:Satellite RNAs promote pancreatic oncogenic processes

| PRJNA337948 | ENA

The ULK3 kinase is a key determinant of keratinocyte self-renewal and tumorigenesis targeting the arginine methylome

Project description:Epigenetic mechanisms oversee epidermal homeostasis and oncogenesis. The identification of kinases controlling these processes has direct therapeutic implications. We show that ULK3 is a nuclear kinase with elevated expression levels in squamous cell carcinomas (SCCs) arising in multiple body sites, including skin and Head/Neck. ULK3 loss by gene silencing or deletion reduces proliferation and clonogenicity of human keratinocytes and SCC-derived cells and affects transcription impinging on stem cell-related and metabolism programs. Mechanistically, ULK3 directly binds and regulates the activity of two histone arginine methyltransferases, PRMT1 and PRMT5 (PRMT1/5), with ULK3 loss compromising PRMT1/5 chromatin association to specific genes and overall methylation of histone H4, a shared target of these enzymes. These findings are of translational significance, as downmodulating ULK3 by RNA interference or locked antisense nucleic acids (LNAs) blunts the proliferation and tumorigenic potential of SCC cells and promotes differentiation in two orthotopic models of skin cancer.

2022-11-14 | MTBLS5155 | MetaboLights

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