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PTENα/β paradoxically promote carcinogenesis through WDR5-H3K4me3 axis [ChIP-seq]

ABSTRACT: PTENα/β paradoxically promote carcinogenesis through WDR5-H3K4me3 axis [ChIP-seq]

PROVIDER: PRJNA524003 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8617056_1.fastq.gz	Fastqsanger.gz
	SRR8617056_2.fastq.gz	Fastqsanger.gz
	SRR8617057_1.fastq.gz	Fastqsanger.gz
	SRR8617057_2.fastq.gz	Fastqsanger.gz
	SRR8617058_1.fastq.gz	Fastqsanger.gz

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PTENα/β paradoxically promote carcinogenesis through WDR5-H3K4me3 axis

Project description:PTENα/β paradoxically promote carcinogenesis through WDR5-H3K4me3 axis

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PTENα/β paradoxically promote carcinogenesis through WDR5-H3K4me3 axis [RNA-seq]

Project description:PTENα/β paradoxically promote carcinogenesis through WDR5-H3K4me3 axis [RNA-seq]

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PTENα/β paradoxically promote carcinogenesis through WDR5-H3K4me3 axis [ChIP-seq]

Project description:we report that USP9X and FBXW11 selectively regulate the stability of PTENα/β but not PTEN proteins by deubiqitination and ubiquitination respectively. USP9X promotes and FBXW11 suppresses tumorigenesis mediated by PTENα/β. In contrast to the current paradigm for PTEN as a tumor suppressor, PTENα/β promote tumorigenesis of cancer cells in a phosphatase-independent manner. Mechanistically, PTENα/β localized in the nucleus regulate expressions of tumor-promoting genes such as NOTCH3 in the similar way as the H3K4 presenter WDR5. Further, PTENα/β but not PTEN directly interact with WDR5 to promote trimethylation of H3K4 and maintain a tumor-promoting signature.

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PTENα/β paradoxically promote carcinogenesis through WDR5-H3K4me3 axis [RNA-seq]

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PTENa/b paradoxically promote carcinogenesis through WDR5-H3K4me3 axis

Project description:PTEN, a widely investigated tumor suppressor, has at least two longer translational variants, PTEN and . However, the regulation and precise roles of endogenous PTEN/ in tumorigenesis remain greatly unknown. Here we show that USP9X and FBXW11 selectively regulate the stability of PTEN/ but not PTEN proteins by deubiqitination and ubiquitination respectively. USP9X promotes and FBXW11 suppresses tumorigenesis mediated by PTEN/. In contrast to the current paradigm for PTEN as a tumor suppressor, PTEN/ promote tumorigenesis of cancer cells in a phosphatase-independent manner. Mechanistically, PTEN/ localized in the nucleus regulate expressions of tumor-promoting genes such as NOTCH3 in the similar way as the H3K4 presenter WDR5. Further, PTEN/ but not PTEN directly interact with WDR5 to promote trimethylation of H3K4 and maintain a tumor-promoting signature. Taken together, our results indicate that PTEN/ are a double-edged sword for carcinogenesis, suggesting that reinterpretation of the importance of PTEN gene in carcinogenesis is warranted.

2019-11-14 | PXD013196 | Pride

PTENa/b paradoxically promote carcinogenesis through WDR5-H3K4me3 axis [RNA-seq 2]

Project description:PTENa/b paradoxically promote carcinogenesis through WDR5-H3K4me3 axis [RNA-seq 2]

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PTENa/b paradoxically promote carcinogenesis through WDR5-H3K4me3 axis [ChIP-seq 2]

Project description:PTENa/b paradoxically promote carcinogenesis through WDR5-H3K4me3 axis [ChIP-seq 2]

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PTENα/β paradoxically promote carcinogenesis through WDR5-H3K4me3 axis

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PTENa/b paradoxically promote carcinogenesis through WDR5-H3K4me3 axis [ChIP-seq 2]

Project description:We report that USP9X and FBXW11 selectively regulate the stability of PTENa/b but not PTEN proteins by deubiquitination and ubiquitination respectively. USP9X promotes and FBXW11 suppresses tumorigenesis mediated by PTENa/b. In contrast to the current paradigm for PTEN as a tumor suppressor, PTENa/b promote tumorigenesis of cancer cells in a phosphatase-independent manner. Mechanistically, PTENa/b localized in the nucleus regulate expressions of tumor-promoting genes such as NOTCH3 in the similar way as the H3K4 presenter WDR5. Further, PTENa/b but not PTEN directly interact with WDR5 to promote trimethylation of H3K4 and maintain a tumor-promoting signature.

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