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HIRA loss transforms FH deficient cells

ABSTRACT: HIRA loss transforms FH deficient cells

PROVIDER: PRJNA838360 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19026570.fastq.gz	Fastqsanger.gz
	SRR19026571.fastq.gz	Fastqsanger.gz
	SRR19026572.fastq.gz	Fastqsanger.gz
	SRR19026573.fastq.gz	Fastqsanger.gz
	SRR19026574.fastq.gz	Fastqsanger.gz

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HIRA loss transforms FH deficient cells [RNA-Seq]

Project description:HIRA loss transforms FH deficient cells [RNA-Seq]

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HIRA loss transforms FH deficient cells [ChIP-Seq]

Project description:HIRA loss transforms FH deficient cells [ChIP-Seq]

| PRJNA838364 | ENA

HIRA loss transforms FH deficient cells [RNA-Seq]

Project description:Purpose: Identifying transcriptional changes led by Hira loss in FH deficient cells Methods: RNA was extracted from the cell lines using QIAGEN kit folloging the manufacturer instructions. RNA concentrator kit was used to guarantee RNA quality. Results/Conclusion: We identified MYC/E2F1 signatures as the top upregulated ones controlling the oncogenic events occuring in Fh1 and Hira deficient cells.

2022-10-29 | GSE201992 | GEO

HIRA loss transforms FH deficient cells [ChIP-Seq]

Project description:Fumarate Hydratase (FH) is a mitochondrial enzyme that catalyses the reversible hydration of fumarate to malate in the TCA cycle. Germline mutations of FH lead to HLRCC, a cancer syndrome characterised by a highly aggressive form of renal cancer(1). Although HLRCC tumours metastasise rapidly, FH-deficient mice develop premalignant cysts in the kidneys, rather than carcinomas(2). How Fh1-deficient cells overcome these tumour suppressive events during transformation is unknown. Here, we perform a genome-wide CRISPR/Cas9 screen to identify genes that, when ablated, enhance the proliferation of Fh1-deficient cells. We found that the depletion of the HIRA enhances proliferation and invasion of Fh1-deficient cells in vitro and in vivo. Mechanistically, Hira loss enables the activation of MYC and its target genes, increasing nucleotide metabolism specifically in Fh1-deficient cells, independent of its histone chaperone activity. These results are instrumental for understanding mechanisms of tumorigenesis in HLRCC and the development of targeted treatments for patients.

2022-10-29 | GSE203056 | GEO

<i>HIRA</i> loss transforms <i>FH</i>-deficient cells.

Project description:Fumarate hydratase (FH) is a mitochondrial enzyme that catalyzes the reversible hydration of fumarate to malate in the tricarboxylic acid (TCA) cycle. Germline mutations of FH lead to hereditary leiomyomatosis and renal cell carcinoma (HLRCC), a cancer syndrome characterized by a highly aggressive form of renal cancer. Although HLRCC tumors metastasize rapidly, FH-deficient mice develop premalignant cysts in the kidneys, rather than carcinomas. How Fh1-deficient cells overcome these tumor-suppressive events during transformation is unknown. Here, we perform a genome-wide CRISPR-Cas9 screen to identify genes that, when ablated, enhance the proliferation of Fh1-deficient cells. We found that the depletion of the histone cell cycle regulator (HIRA) enhances proliferation and invasion of Fh1-deficient cells in vitro and in vivo. Mechanistically, Hira loss activates MYC and its target genes, increasing nucleotide metabolism specifically in Fh1-deficient cells, independent of its histone chaperone activity. These results are instrumental for understanding mechanisms of tumorigenesis in HLRCC and the development of targeted treatments for patients.

| S-EPMC9586478 | biostudies-literature

HIRA loss transforms FH deficient cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-10-29 | GSE203057 | GEO

Genome-wide expression profile in FH-deficient vs FH-competent cells

Project description:Genome-wide expression profile in FH-deficient vs FH-competent cells

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Genome-wide expression profile in FH-deficient (UOK262) vs FH-competent (UOK262pFH) human cells derived from metastatsis to the mediastinum of a HLRCC patient

Project description:Comparison of the transcriptome of human kideny cancer cells either wild-type for FH or FH-deficient. The UOK262 cells were isolated from mediastinum metastasis of a HLRCC patient (Yang et al. Cancer Genetics and Cytogenetics, Volume 196, Issue 1, 1 January 2010, Pages 45–55). FH function was restored in the UOK262 by re-expressing the FH transcript from an exogenous plasmid.

2016-09-22 | GSE77538 | GEO

Comprehensive molecular profiling of FH-deficient renal cell carcinoma identifies molecular subtypes and novel therapeutic targets

Project description:Conducting an in-depth exploration of the multi-omics landscape of Fumarate Hydratase (FH)-deficient renal cell carcinoma (RCC), the study aimed to unravel the intricate molecular mechanisms underlying this rare and aggressive form of renal cancer. Analyzing 126 patients with FH-deficient RCC, we identified distinct variant spectrum of FH gene, with truncating mutation correlated with adverse prognostic factors and a worse response to immune checkpoint blockade. The identification of three molecular subtypes with diverse clinical/genomic characteristics and varying response to systemic treatment further enriched the understanding of the heterogeneous tumor microenvironment (particularly immune-related) in FH-deficient RCC, and suggested potential therapeutic targets. These findings offer a basis for molecular stratification, shedding light on the tailored therapeutic strategies in improving treatment response of FH-deficient RCC.

2025-03-06 | GSE291073 | GEO

Expression data from mouse kidney epithelial cells

Project description:Fumarate hydratase (FH) is the enzyme in the Krebs cycle, which transforms fumarate to malate. Loss of fumarate hyrdragase leads to hereditary leiomyomatosis and renal cell cancer (HLRCC). The biallelic inactivation has been highly accumulated in FH-deficient cells and is considered a major pro-oncogenic factor for HLRCC tumorigenesis. We used microarrays to understand the global readaptation of cell metabolism of gene expression underlying the truncated Krebs cycle by loss of function of fumarate hydratase. The fumarate hydratase wild type and knock out cells were generated for RNA extraction and hybridization on Affymetrix microarrays.

2014-11-19 | E-GEOD-63438 | biostudies-arrayexpress

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