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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE135478 | GEO | 2019/10/17

REPOSITORIES: GEO

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

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

| PRJNA524001 | ENA