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The WDR5-H3K4me3 epigenetic axis regulates OPN expression to compensate PD-L1 function to promote pancreatic cancer immune escape [ChIP-seq]

ABSTRACT: The WDR5-H3K4me3 epigenetic axis regulates OPN expression to compensate PD-L1 function to promote pancreatic cancer immune escape [ChIP-seq]

PROVIDER: PRJNA740000 | ENA |

REPOSITORIES: ENA

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The WDR5-H3K4me3 epigenetic axis regulates OPN expression to compensate PD-L1 function to promote pancreatic cancer immune escape [RNA-seq]

Project description:Two orthotopic pancreatic tumor mouse models were used for ChIP-Seq and RNA-Seq to identify genome-wide dysfunction of H3K4me3 and gene expression. Mouse pancreatic tumors have a genome-wide increase in H3K4me3 deposition as compared to normal pancreas. Osteopontin (OPN) and its receptor CD44 were identified being up-regulated in pancreatic tumors by their promoter H3K4me3 deposition. OPN protein is increased in both tumor cells and tumor-infiltrating immune cells in human pancreatic carcinoma and is inversely correlated with pancreatic cancer patient survival. OPN is primarily expressed in tumor cells and monocytic myeloid-derived suppressor cells (M-MDSCs), whereas PD-L1 is expressed in tumor cells, M-MDSCs, polymorphonuclear MDSCs (PMN-MDSCs) and tumor-associated macrophages. WDR5 is essential for H3K4me3-specific histone methyltransferase activity and OPN expression in tumor cells and MDSCs. Pharmacological inhibition of WDR5 significantly decreased OPN protein level, suppressed pancreatic tumor growth, and significantly increased efficacy of anti-PD-1 immunotherapy in suppression of pancreatic tumor growth in vivo.

2021-07-09 | GSE178676 | GEO

The WDR5-H3K4me3 epigenetic axis regulates OPN expression to compensate PD-L1 function to promote pancreatic cancer immune escape

Project description:The WDR5-H3K4me3 epigenetic axis regulates OPN expression to compensate PD-L1 function to promote pancreatic cancer immune escape

| PRJNA739994 | ENA

The WDR5-H3K4me3 epigenetic axis regulates OPN expression to compensate PD-L1 function to promote pancreatic cancer immune escape [RNA-seq]

Project description:The WDR5-H3K4me3 epigenetic axis regulates OPN expression to compensate PD-L1 function to promote pancreatic cancer immune escape [RNA-seq]

| PRJNA740002 | ENA

WDR5-H3K4me3 epigenetic axis regulates OPN expression to compensate PD-L1 function to promote pancreatic cancer immune escape.

Project description: Not available

| S-EPMC8323468 | biostudies-literature

The WDR5-H3K4me3 epigenetic axis regulates OPN expression to compensate PD-L1 function to promote pancreatic cancer immune escape

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

2021-07-09 | GSE178677 | GEO

The WDR5-H3K4me3 epigenetic axis regulates OPN expression to compensate PD-L1 function to promote pancreatic cancer immune escape [ChIP-seq]

Project description:Total RNA was isolated from normal C57BL/6 mouse pancreas, PANC02-H7, and UN-KC-6141 tumors from tumor-bearing mice. The RNA was used for RNA-Seq. The gene expression profiles between normal mouse pancreas and orthotopic pancreatic tumors were compared, and differentially expressed genes were identified.

2021-07-09 | GSE178675 | GEO

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

Wdr5

Project description:Wdr5

| PRJNA739648 | ENA

Genome profiling of WDR5 and H3K4me3 binding in mouse embryonic stem cells

Project description:This study describes the binding profile of WDR5 and H3K4me3 in Wdr5 and p53 double knockout ESC rescued with WDR5WT or WDR5S91KY191F

2021-06-22 | GSE178552 | GEO

Genome profiling of WDR5, P53, H3K4Me3 binding in mouse embryonic bodies using SFEBq differetiation methods

Project description:This study describes the binding profile of WDR5, p53 and H3K4Me3 in mouse embryonic bodies at day 2 (WT, Wdr5 KO, Wdr5 and p53 double knockout)

2019-11-25 | GSE140899 | GEO

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