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USP37 Promotes Deubiquitination of HIF2a in Kidney Cancer

ABSTRACT: USP37 Promotes Deubiquitination of HIF2a in Kidney Cancer

PROVIDER: PRJNA627118 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11579359_1.fastq.gz	Fastqsanger.gz
	SRR11579359_2.fastq.gz	Fastqsanger.gz
	SRR11579360_1.fastq.gz	Fastqsanger.gz
	SRR11579360_2.fastq.gz	Fastqsanger.gz
	SRR11579361_1.fastq.gz	Fastqsanger.gz

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USP37 Promotes Deubiquitination of HIF2a in Kidney Cancer

Project description:Clear cell renal cell carcinoma (ccRCC) is characterized by a loss of tumor suppressor Von Hippel Lindau (VHL) function, which leads to accumulation of hypoxia inducible factor (including HIF1 and HIF2). HIF2 was previously reported to be one of the major oncogenic drivers in ccRCC, however its therapeutic targeting remains challenging. Here we performed a deubiquitinase (DUB) cDNA library binding screen and discovered that USP37 is a DUB that binds HIF2 and promotes HIF2 deubiquitination. As a result, USP37 promotes HIF2 protein stability in an enzymatically dependent manner and depletion of USP37 leads to HIF2 downregulation in ccRCC. Functionally, USP37 depletion causes decreased cell proliferation measured by MTS, 2-D colony formation as well as 3-D anchorage independent growth. USP37 is also essential for maintaining kidney tumorigenesis in an orthotopic xenograft model and its depletion leads to decreased primary kidney tumorigenesis and spontaneous lung metastasis. Our results suggest that USP37 is a potential new therapeutic target in ccRCC.

2020-05-27 | GSE149005 | GEO

USP13 Promotes Deubiquitination of ZHX2 and Tumorigenesis in Kidney Cancer

Project description:USP13 Promotes Deubiquitination of ZHX2 and Tumorigenesis in Kidney Cancer

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USP13 Promotes Deubiquitination of ZHX2 and Tumorigenesis in Kidney Cancer

Project description:Clear cell renal cell carcinoma (ccRCC) is characterized by loss of tumor suppressor Von Hippel Lindau (VHL) function. VHL is the component of E3 ligase complex that promotes the ubiquitination and degradation of hypoxia inducible factor alpha (including HIF1alpha and HIF2alpha) and Zinc Fingers And Homeoboxes 2 (ZHX2). Our recent research showed that ZHX2 contributed to ccRCC tumorigenesis in a HIF independent manner. However, it remains unknown whether ZHX2 can be regulated through deubiquitination. Here we performed a deubiquitinase (DUB) cDNA library binding screen and identified USP13 as a novel DUB that bound ZHX2 and promoted ZHX2 deubiquitination. As a result, USP13 promoted ZHX2 protein stability in an enzymatically dependent manner and depletion of USP13 led to ZHX2 downregulation in ccRCC. Functionally, USP13 depletion led to decreased cell proliferation measured by 2-D colony formation and 3-D anchorage independent growth. USP was a critical effector on maintaining kidney tumorigenesis in an orthotopic xenograft model and its depletion led to both decreased primary kidney tumorigenesis and spontaneous lung metastasis. Our results suggest that USP13 is a potential new therapeutic target in ccRCC.

2022-07-27 | GSE186717 | GEO

Expression data from HIF2A WT vs KD Madin-Darby canine kidney epithelial cells (MDCK strain II cells (ATCC:CCL-34)) under normoxic and hypoxic conditions

Project description:No one pathway was identified in up- and downregulated genes profile in HIF2A KD Madin-Darby canine kidney epithelial cells (MDCKII) in normoxic condition. We used microarray to study the differential expression of genes in HIF2A knockdown versus WT Madin-Darby canine kidney epithelial cells (MDCKII)

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YOD1 promotes renal fibrosis by stabilizing JAK2 through deubiquitination

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Project description:HIF2a function is both necessary and sufficient for the growth of VHL-null clear cell Renal Cell Carcinoma (ccRCC). Targeting HIF2a function can therefore be a promising therapeutic strategy. We used microarray analysis to characterize a novel pharmacological inhibitor of HIF2a named PT2399. By comparing genes that are responsive to PT2399 in parental cells vs cells lacking HIF2a, by virtue of CRISPR-mediated genetic editing, we characterized gene signatures that are regulated by PT2399 in a HIF2a dependent manner. Cells were treated with either DMSO (control) or 2uM PT2399 for indicated time periods, total RNA was extracted and analyzed. Please note that the experiments with 786O Parental and HIF2a null cells were conducted independently.

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