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BMAL1-HIF2α heterodimers contribute to ccRCC

ABSTRACT: BMAL1-HIF2α heterodimers contribute to ccRCC

PROVIDER: PRJNA1229506 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32512433_1.fastq.gz	Fastqsanger.gz
	SRR32512433_2.fastq.gz	Fastqsanger.gz
	SRR32512434_1.fastq.gz	Fastqsanger.gz
	SRR32512434_2.fastq.gz	Fastqsanger.gz
	SRR32512435_1.fastq.gz	Fastqsanger.gz

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BMAL1-HIF2α heterodimers contribute to ccRCC

Project description:Circadian disruption enhances cancer risk, and many tumors exhibit disordered circadian gene expression. We show rhythmic gene expression is unexpectedly robust in clear cell renal cell carcinoma (ccRCC). Furthermore, the clock gene BMAL1 is higher in ccRCC than in healthy kidneys, unlike in other tumor types. BMAL1 is closely related to ARNT and we show that BMAL1-HIF2α regulates a subset of HIF2α target genes in ccRCC cells. Depletion of BMAL1 reprograms HIF2α chromatin association and target gene expression and reduces ccRCC growth in culture and in xenografts. Analysis of pre-existing data reveals higher BMAL1 in patient-derived xenografts that are sensitive to growth suppression by HIF2α antagonists. We show that increasing BMAL1 sensitizes ccRCC-derived A498 cells to growth inhibition by PT2399. Together, these findings indicate that an alternate HIF2α heterodimer containing the circadian partner BMAL1 contributes to HIF2α activity, growth, and sensitivity to HIF2α antagonist drugs in ccRCC cells.

2025-03-17 | GSE290669 | GEO

BMAL1-HIF2α heterodimers contribute to ccRCC [RNA-seq]

Project description:BMAL1-HIF2α heterodimers contribute to ccRCC [RNA-seq]

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BMAL1-HIF2α heterodimers contribute to ccRCC [ChIP-seq]

Project description:BMAL1-HIF2α heterodimers contribute to ccRCC [ChIP-seq]

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BMAL1-HIF2α heterodimers contribute to ccRCC [RNA-seq_FigS6]

Project description:BMAL1-HIF2α heterodimers contribute to ccRCC [RNA-seq_FigS6]

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BMAL1-HIF2α heterodimers contribute to ccRCC [RNA-seq_FigS4]

Project description:BMAL1-HIF2α heterodimers contribute to ccRCC [RNA-seq_FigS4]

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BMAL1-HIF2α heterodimers contribute to ccRCC [RNA-seq_Fig2]

Project description:BMAL1-HIF2α heterodimers contribute to ccRCC [RNA-seq_Fig2]

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BMAL1-HIF2α heterodimers contribute to ccRCC [RNA-seq]

2025-05-08 | GSE290779 | GEO

BMAL1-HIF2α heterodimers contribute to ccRCC [ChIP-seq]

Project description:Circadian disruption enhances cancer risk, and many tumors exhibit disordered circadian gene expression. We show rhythmic gene expression is unexpectedly robust in clear cell renal cell carcinoma (ccRCC). Furthermore, the clock gene BMAL1 is higher in ccRCC than in healthy kidneys, unlike in other tumor types. BMAL1 is closely related to ARNT and we show that BMAL1-HIF2α regulates a subset of HIF2α target genes in ccRCC cells. Depletion of BMAL1 reprograms HIF2α chromatin association and target gene expression and reduces ccRCC growth in culture and in xenografts. Analysis of pre-existing data reveals higher BMAL1 in patient-derived xenografts that are sensitive to growth suppression by HIF2α antagonists. We show that increasing BMAL1 sensitizes ccRCC-derived 786O cells to growth inhibition by PT2399. Together, these findings indicate that an alternate HIF2α heterodimer containing the circadian partner BMAL1 contributes to HIF2α activity, growth, and sensitivity to HIF2α antagonist drugs in ccRCC cells.

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BMAL1-HIF2α heterodimers contribute to ccRCC [RNA-seq_FigS6]

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BMAL1-HIF2α heterodimers contribute to ccRCC [RNA-seq_FigS4]

Project description:Circadian disruption enhances cancer risk, and many tumors exhibit disordered circadian gene expression. We show rhythmic gene expression is unexpectedly robust in clear cell renal cell carcinoma (ccRCC). Furthermore, the clock gene BMAL1 is higher in ccRCC than in healthy kidneys, unlike in other tumor types. BMAL1 is closely related to ARNT and we show that BMAL1-HIF2α regulates a subset of HIF2α target genes in ccRCC cells. Depletion of BMAL1 reprograms HIF2α chromatin association and target gene expression and reduces ccRCC growth in culture and in xenografts. Analysis of pre-existing data reveals higher BMAL1 in patient-derived xenografts that are sensitive to growth suppression by HIF2α antagonists. We show that increasing BMAL1 sensitizes ccRCC-derived 786O cells to growth inhibition by PT2399. Together, these findings indicate that an alternate HIF2α heterodimer containing the circadian partner BMAL1 contributes to HIF2α activity, growth, and sensitivity to HIF2α antagonist drugs in ccRCC cells.

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