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Regulatory consequences of ZNF395 knock-down in MDA-LM2-shTARBP2 cell-line

ABSTRACT: shRNA-mediated knock-down followed by transcriptomic profiling revealed that silencing of ZNF395 resulted in a significant up-regulation in several key oncogenes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE49613 | GEO | 2014/07/24

SECONDARY ACCESSION(S): PRJNA214601

REPOSITORIES: GEO

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Regulatory consequences of ZNF395 knock-down in MDA-LM2-shTARBP2 cell-line

Project description:shRNA-mediated knock-down followed by transcriptomic profiling revealed that silencing of ZNF395 resulted in a significant up-regulation in several key oncogenes. ZNF395 was knocked-down, via expression of short-hairpin RNAs targeting its transcript. The cells were then subjected to transcripome profiling in comparison to mock-transfected cells.

2014-07-24 | E-GEOD-49613 | biostudies-arrayexpress

Regulatory consequences of SOX4 knock-down in MDA-LM2 cell line

Project description:Transcriptomic profiling of SOX4 knock-down MDA-LM2 cell line resulted in down-regulation of its transcriptional target gene, TMEM2.

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Regulatory consequences of TARBP2 knock-down in MDA-LM2 cell-line

Project description:siRNA-mediated knock-down followed by transcriptomic profiling revealed that silencing of TARBP2 resulted in a significant up-regulation of sRSE-carrying transcripts.

2014-07-24 | GSE49611 | GEO

Regulatory consequences of SOX4 knock-down in MDA-LM2 cell line

Project description:Transcriptomic profiling of SOX4 knock-down MDA-LM2 cell line resulted in down-regulation of its transcriptional target gene, TMEM2. Two independent siRNAs were used to knock down SOX4 in metastatic MDA-LM2 cells. The cells were then subjected to transcripome profiling in comparison to control siRNA-transfected cells.

2016-03-15 | E-GEOD-79202 | biostudies-arrayexpress

Regulatory consequences of TARBP2 knock-down in MDA-LM2-shDicer cell-line

Project description:siRNA-mediated knock-down followed by transcriptomic profiling revealed that silencing of TARBP2 resulted in a significant up-regulation of sRSE-carrying transcripts.

2014-07-24 | GSE56950 | GEO

Regulatory consequences of TARBP2 knock-down in MDA-LM2 cell-line

Project description:siRNA-mediated knock-down followed by transcriptomic profiling revealed that silencing of TARBP2 resulted in a significant up-regulation of sRSE-carrying transcripts. Two independent siRNAs were used to knock down TARBP2 in metastatic MDA-LM2 cells. The cells were then subjected to transcripome profiling in comparison to mock-transfected cells.

2014-07-24 | E-GEOD-49611 | biostudies-arrayexpress

Regulatory consequences of TARBP2 knock-down in MDA-LM2-shDicer cell-line

Project description:siRNA-mediated knock-down followed by transcriptomic profiling revealed that silencing of TARBP2 resulted in a significant up-regulation of sRSE-carrying transcripts. Two independent siRNAs were used to knock down TARBP2 in metastatic MDA-LM2 shDicer cells. The cells were then subjected to transcripome profiling in comparison to mock-transfected cells.

2014-07-24 | E-GEOD-56950 | biostudies-arrayexpress

Regulatory consequences of TARBP2 knock-down in MDA-LM2 cell-line [stability experiment]

2014-07-24 | GSE49612 | GEO

Regulatory consequences of TARBP2 knock-down in MDA-LM2 cell-line [stability experiment]

Project description:siRNA-mediated knock-down followed by transcriptomic profiling revealed that silencing of TARBP2 resulted in a significant increase in the stability of sRSE-carrying transcripts. Two independent siRNAs were used to knock down TARBP2 in metastatic MDA-LM2 cells. The cells were then subjected to whole-genome transcript stabiliy measurements in comparison to mock-transfected cells.

2014-07-24 | E-GEOD-49612 | biostudies-arrayexpress

Genome-wide chromatin profiles of ZNF395 [RNA-seq]

Project description:Hypoxia signaling induced by VHL deficiency fuels growth but also poses immense metabolic stress to clear cell renal cell carcinomas (ccRCCs). Tumor cells depend on glutamine as the primary source of tricarboxylic acid (TCA) anaplerosis. Hypoxia-inducible factor alpha (HIFα) governs glycolysis but does not directly regulate glutamine metabolism; instead, the factor responsible for orchestrating glutamine metabolism and mitochondrial adaptations to hypoxia remains elusive. We now show that ZNF395 is a hypoxia-responsive factor that regulates glutamine metabolism in the mitochondria. ZNF395 is activated by a HIF2α-modulated super-enhancer but plays non-redundant functions from HIF2α. Specifically, ZNF395 facilitates the transcription of enzymes essential for glutaminolysis, including glutaminase (GLS) and isocitrate dehydrogenase 2 (IDH2). Functionally, ZNF395 depletion results in reduced TCA intermediates and their derivatives, including amino acids, glutathione and pyrimidine nucleotides. In addition, ZNF395 depletion diminishes mitochondrial respiration; restoration of complex I function rescues the effects of ZNF395 depletion. Our study underscores the coordinated role of HIFα and ZNF395 in shaping metabolic adaptations in response to hypoxia in VHL-deficient ccRCCs.

2024-10-01 | GSE247117 | GEO

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