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Status |
Public on Oct 17, 2019 |
Title |
PTENa/b paradoxically promote carcinogenesis through WDR5-H3K4me3 axis [RNA-seq 2] |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by high throughput sequencing
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Summary |
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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Overall design |
RNA sequencing in SMMC-7721 cell lines with or without WDR5 depletion by two independent experiments.
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Contributor(s) |
Shen SM, Zhang C, Ge MK, Dong SS |
Citation(s) |
31685992 |
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Submission date |
Aug 06, 2019 |
Last update date |
Jan 16, 2020 |
Contact name |
ge mengkai |
E-mail(s) |
[email protected]
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Phone |
15201867201
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Organization name |
Shanghai Jiao Tong University School of Medicine (SJTU-SM)
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Street address |
shanghai
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City |
shanghai |
State/province |
State... |
ZIP/Postal code |
13185541251gmk |
Country |
China |
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Platforms (1) |
GPL24676 |
Illumina NovaSeq 6000 (Homo sapiens) |
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Samples (4)
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This SubSeries is part of SuperSeries: |
GSE126984 |
PTENα/β paradoxically promote carcinogenesis through WDR5-H3K4me3 axis |
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Relations |
BioProject |
PRJNA559007 |
SRA |
SRP217604 |