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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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			Action	DRS
	SRR15242575_1.fastq.gz	Fastqsanger.gz
	SRR15242575_2.fastq.gz	Fastqsanger.gz
	SRR15242576_1.fastq.gz	Fastqsanger.gz
	SRR15242576_2.fastq.gz	Fastqsanger.gz
	SRR15242577_1.fastq.gz	Fastqsanger.gz

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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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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.

2021-10-11 | GSE180797 | GEO

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

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

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Mutations in splicing factor SF3B1 promote transformation through MYC stabilization

Project description:Although mutations in the RNA splicing factor SF3B1 are frequently observed in multiple human cancers, their functional role in promoting tumorigenesis and therapeutic significance remain poorly understood. Here we characterize the splicing landscape of 79 tumors and 12 isogenic cell lines harboring SF3B1 hotspot mutations, identifying hundreds of cryptic 3’ splice site (ss) events shared as well as specific to different tumor types. Regulatory network analysis shows that tumors harboring the most common hotspot mutation in SF3B1 (SF3B1K700E) activate the MYC transcriptional program. SF3B1 mutations lead to a dramatic decay of transcripts encoding the key PP2A phosphatase subunit PPP2R5A due to aberrant 3’ss usage, resulting in increased c-MYC serine 62 phosphorylation (allowing MYC to escape ubiquitin-mediated degradation) and in increased BCL2 serine 70 phosphorylation (leading to anti-apoptotic effects). This effect of SF3B1K700E on c-MYC and BCL2 activation through post-translational regulation was conserved across human and mouse cells and could be rescued by restored expression of PPP2R5A. Consonant with this, mutant SF3B1 promoted c-MYC driven tumorigenesis could be restored by the PP2A activating agent FTY-720. This study reveals the functional contribution of mutant SF3B1 to tumorigenesis through regulation of established oncogenic pathways and provides therapeutic strategies for related tumors.

2020-05-01 | GSE116391 | GEO

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

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

Project description:The significance of MYC deregulation has been well-documented in T-cell acute lymphoblastic leukemia (T-ALL). MYC acts as an oncogenic driver in T-ALL and particularly in maintaining leukemia-initiating cell activity. Protein interactome analysis identified Aurora B kinase (AURKB) as a specific MYC binding partner and depletion of AURKB reduced the steady-state levels of MYC. Mechanistic studies demonstrated that AURKB directly phosphorylated MYC and promoted MYC protein stability, and conversely AURKB deficiency elicited rapid MYC degradation. We thus predicted that abrogation of AURKB would affect global MYC transcriptional program. To assess the transcriptional change in response to AURKB knockdown, RNA-Seq was performed using AURKB or control-depleted CUTLL1 cells.

2020-02-11 | GSE140739 | GEO

Peri-pubertal High-Fat Diet Promotes c-Myc Stabilization in Mammary Gland Epithelium

Project description:Dietary fat consumption during rapid mammary gland developing period such as peri-pubertal maturation or pregnancy increases the risk for breast cancer. However, the molecular mechanism underlying this observation is not well elucidated. To provide mechanistic insight, we examined gene expression profile in mouse mammary epithelial cells (MMECs) exposed to high-fat diet (HFD) or control diet (CD). Trp53-/- female mice were treated with experimental diets for 5 weeks during the peri-puberty period (3 to 8 weeks of age). This treatment induced insignificant difference in body weight between mice exposed to HFD and CD. Gene Set Enrichment Analysis (GSEA) predicted elevated expression of c-Myc target genes when exposed to HFD. Consistently, we detected marked elevation of c-Myc protein and prolongation of its half-life in MMECs exposed to HFD suggesting that HFD increased its stability. Additionally, we observed increased phosphorylation at c-MycS62 with concomitant increase in ERK phosphorylation. HFD rendered Trp53-/- MMECs more colonogenic and spherogenic, which was antagonized by a c-Myc inhibitor. Oleic acid the main fatty acid constituent of the HFD and TAK-875 an agonist for G protein-coupled receptor 40 (a receptor for oleic acid) as well enhanced c-Myc stabilization and MMECs proliferation. Collectively, these data suggest that HFD exerts its effect on MMECs through the stabilization of an oncoprotein, deciphering a novel mechanism whereby dietary fat promotes mammary carcinogenesis.

2020-05-24 | GSE144328 | GEO

Astrocyte elevated gene-1 (AEG-1) and c-Myc cooperate to promote hepatocarcinogenesis

Project description:Double transgenic mice with hepatocyte-specific expression of AEG-1 and c-Myc show aggressive HCC compared to single transgenics. Gene expression was analyzed to understand the molecular mechanism by which AEG-1 and c-Myc cooperate to promote hepatocarcinogenesis. Livers were collected from naïve adult mice (3 mice/group). Total RNA was extrancted and subjected to RNA-Seq.

2014-09-30 | E-GEOD-61875 | biostudies-arrayexpress

Combined BET bromodomain and CDK2 inhibition in MYC-driven medulloblastoma

Project description:MYC genes are frequently amplified and correlate with poor prognosis in MB. BET bromodomains recognize acetylated lysine residues and often promote and maintain MYC transcription. Certain cyclin-dependent kinases (CDKs) are further known to support MYC stabilization in tumor cells. In this report, MB cells were suppressed by combined targeting of MYC expression and MYC stabilization using BET bromodomain inhibition and CDK2 inhibition, respectively. Such combination treatment worked synergistically and caused cell cycle arrest as well as massive apoptosis. Immediate transcriptional changes from this combined MYC blockade were found using RNA-Seq profiling and showed remarkable similarities to changes in MYC target gene expression when MYCN was turned off with doxycycline in our MYCN-inducible animal model for Group 3 MB. In addition, the combination treatment significantly prolonged survival as compared to single agent therapy in orthotopically transplanted human Group 3 MB with MYC amplifications. Our data suggests that dual inhibition of CDK2 and BET bromodomains can be a novel treatment approach for suppressing MYC-driven cancer.

2018-06-06 | GSE107405 | GEO

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