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USP29 coordinates MYC and HIF1α stabilization to promote tumor metabolism and progression

ABSTRACT: USP29 coordinates MYC and HIF1α stabilization to promote tumor metabolism and progression

PROVIDER: PRJNA749584 | ENA |

REPOSITORIES: ENA

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USP29 coordinates MYC and HIF1α stabilization to promote tumor metabolism and progression

Project description:Deleption of USP29 significantly inhibits aerobic glycolysis, glutamine catabolism and proliferation of cancer cells. To test the underlying mechanisms, RNA-seq was performed using USP29 or control depleted SK-N-BE2 and Ramos cells.

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Mutations in splicing factor SF3B1 promote transformation through MYC stabilization

Project description:Mutations in splicing factor SF3B1 promote transformation through MYC stabilization

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Direct Phosphorylation and Stabilization of MYC by Aurora B Kinase Promote T Cell Leukemogenesis

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miRNA expression in primary renal carcinomas, subgrouped based on HIF1α expression

Project description:Clear cell renal cell carcinoma (ccRCC), the most common type of renal cancer is often associated with inactivation of the tumor suppressor gene von-Hippel Lindau (VHL), leading to stable expression of hypoxia inducible factors, HIF1α and HIF2α. Although HIF1α functions as a tumor suppressor gene, majority of ccRCCs constitutively express HIF1α, stratifying VHL-deficient ccRCCs into groups which express either both HIF1α and HIF2α (H1H2) or HIF2α exclusively (H2). MicroRNA (miRNA) profiling performed in these two ccRCC subtypes to identify novel molecular mechanisms. ccRCCs were classified into H1H2 and H2 subtypes by immunohostochemical staining of H1F1α and H1F2α expression. Five H1H2 tumor samples and eight H2 tumor samples were used for the study. Matched adjacent normal renal tissues were used as respective controls.

2013-09-30 | E-GEOD-47582 | biostudies-arrayexpress

Identification of interacting proteins of lncRNA HIF1α-AS1

Project description:LncRNA Hypoxia-inducible factor 1α-antisense 1 (HIF1α-AS1) is located on the antisense strand of the important Hypoxia-inducible factor 1α (HIF1α) gene, but being transcribed in antisense direction along the HIF1α promoter. Here we used the 3’end biotinylated HIF1a-AS1 RNA and a control RNA for RNA Pulldown and searched for interacting proteins in nuclear extracts of human umbilical vein endothelial cells (HUVEC).

2022-09-23 | PXD023512 | Pride

Development of gene expression signatures for WT (Hif1afl/fl) mice and VSMC-specific HIF1α disruption (Hif1a△SMC) mice VSMCs treated with 150μM CoCl2 for 24hours

Project description:HIF1α is a key regulator of hypoxia, however, the changes of its target genes in VSMCs under hypoxia were unknown. CoCl2 is a chemical hypoxia agent which leads to the stabilization of HIF1-α and the expression of hypoxia responsive genes, Therefore Hif1afl/fl and Hif1a△SMC VSMCs were treated with CoCl2 and performed microarray analysis. We used microarray to detail the gene expression of WT (Hif1afl/fl) mice and VSMC-specific HIF1α disruption (Hif1a△SMC) mice VSMCs treated with 150μM CoCl2 for 24hours.

2020-06-22 | GSE119226 | GEO

Hif1α down-regulation is associated with transposition of great arteries in mice treated with a RA antagonist

Project description:Aims: Congenital heart defect (CHD) account for 25% of all human congenital abnormalities. Very few CHD-causing genes have been identified so far; so, to discover further genes we performed a global transcriptome analysis in mouse models of CHD. Methods and results: By the use of a retinoic acid competitive antagonist (BMS-189453) we caused CHD, thymic abnormalities and neural tube defects in mouse newborns. Transposition of great arteries was the prevalent cardiac defect observed (61%). Recently we were able to partially rescue this abnormal phenotype by oral administration of folic acid. Now we have performed a microarray analysis in mouse embryos (8.5 dpc) treated with BMS-189453 alone and with BMS-189453 plus folic acid (FA). On the basis of microarray and QRT-PCR results, we deeper analysed Hif1α because of its down-regulation in BMS-treated embryos vs WT and its increased expression level in BMS+FA treated embryos compared to BMS-treated ones. Immunofluorescence experiments confirmed the under-expression of Hif1α protein in BMS-treated embryos compared to WT and BMS+FA treated ones and moreover demonstrated that at 8.5 dpc Hif1α is mainly expressed in the embryo’s heart. Conclusion: We propose that Hif1α down-regulation by blocking retinoic acid binding, may contribute to the development of the cardiac defects of mouse newborns. In line with our hypothesis, when Hif1α expression level is restored (by supplementation of folic acid) a decrement of CHD is found. At the best of our knowledge this is the first report that link retinoic acid metabolism to Hif1α regulation and the development of TGA 2 samples w/ 2 dye-swaps

2010-09-20 | E-GEOD-19012 | biostudies-arrayexpress

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The transcriptome and genome-wide mapping of Hif1α binding sites in kidney tubule cells

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PHF5A coordinates p300 for epigenetic regulation of lipogenesis to promote hepatocellular carcinoma progression

Project description:PHF5A coordinates p300 for epigenetic regulation of lipogenesis to promote hepatocellular carcinoma progression

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