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An epigenetic mechanism underlying chromosome 17p deletion-driven tumorigenesis

ABSTRACT: An epigenetic mechanism underlying chromosome 17p deletion-driven tumorigenesis

PROVIDER: PRJNA606276 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11074300_1.fastq.gz	Fastqsanger.gz
	SRR11074300_2.fastq.gz	Fastqsanger.gz
	SRR11074301_1.fastq.gz	Fastqsanger.gz
	SRR11074301_2.fastq.gz	Fastqsanger.gz
	SRR11074302_1.fastq.gz	Fastqsanger.gz

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An epigenetic mechanism underlying chromosome 17p deletion-driven tumorigenesis

Project description:Chromosome copy number variations are a hallmark of human cancers and among them chromosome 17p loss is the most common one and associated with poor prognosis. Our previous work demonstrates that 17p deletions can promote tumorigenesis more than p53 loss. Herein, with multiple functional genetic strategies, we identify a new 17p tumor suppressor, PHD finger protein 23 (PHF23). PHF23 deficiency impaires B cell differentiation and promotes Myc-driven lymphoma. Mechanistically, PHF23, a H3K4me3 reader, directly binds and represses the deacetylation activity of the SIN3-HDAC complex through its N-terminus, which coordinates two major active histone markers H3K4me3 and H3K27ac for activation of downstream B cell-differentiation genes and tumor suppressors. Further, we show that dysregulation of the PHF23-SIN3-HDAC complex is essential for PHF23 deficiency-induced tumorigenesis and maintenance. Hence, our study reveals a novel epigenetic regulatory mechanism that contributed to the pathology of 17p deleted cancers and suggests novel susceptibility of this miserable disease.

2020-12-20 | GSE145190 | GEO

An Epigenetic Mechanism Underlying Chromosome 17p Deletion-Driven Tumorigenesis.

Project description:Chromosome copy-number variations are a hallmark of cancer. Among them, the prevalent chromosome 17p deletions are associated with poor prognosis and can promote tumorigenesis more than TP53 loss. Here, we use multiple functional genetic strategies and identify a new 17p tumor suppressor gene (TSG), plant homeodomain finger protein 23 (PHF23). Its deficiency impairs B-cell differentiation and promotes immature B-lymphoblastic malignancy. Mechanistically, we demonstrate that PHF23, an H3K4me3 reader, directly binds the SIN3-HDAC complex through its N-terminus and represses its deacetylation activity on H3K27ac. Thus, the PHF23-SIN3-HDAC (PSH) complex coordinates these two major active histone markers for the activation of downstream TSGs and differentiation-related genes. Furthermore, dysregulation of the PSH complex is essential for the development and maintenance of PHF23-deficient and 17p-deleted tumors. Hence, our study reveals a novel epigenetic regulatory mechanism that contributes to the pathology of 17p-deleted cancers and suggests a susceptibility in this disease. SIGNIFICANCE: We identify PHF23, encoding an H3K4me3 reader, as a new TSG on chromosome 17p, which is frequently deleted in human cancers. Mechanistically, PHF23 forms a previously unreported histone-modifying complex, the PSH complex, which regulates gene activation through a synergistic link between H3K4me3 and H3K27ac.This article is highlighted in the In This Issue feature, p. 1.

| S-EPMC8591992 | biostudies-literature

REQUIREMENT FOR PKC EPSILON IN KRAS-DRIVEN LUNG TUMORIGENESIS

Project description:REQUIREMENT FOR PKC EPSILON IN KRAS-DRIVEN LUNG TUMORIGENESIS

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REQUIREMENT FOR PKC EPSILON IN KRAS-DRIVEN LUNG TUMORIGENESIS

Project description:Non-small cell lung cancer (NSCLC), the most frequent subtype of lung cancer, remains a highly lethal malignancy and one of the leading causes of cancer deaths worldwide. Mutant KRAS is the prevailing oncogenic driver of lung adenocarcinoma, the most common histological form of NSCLC. In this study, we examined the role of PKCe, an oncogenic kinase highly expressed in NSCLC and other cancers, in KRAS-driven tumorigenesis. Notably, database analysis revealed an association between PKCe expression and poor outcome in lung adenocarcinoma patients specifically having KRAS mutation. By generating a PKCe-deficient, conditionally activatable allele of oncogenic Kras (LSL-Kras G12D ;PKCe -/- mice) we were able to demonstrate the requirement of PKCe for Kras-driven lung tumorigenesis in vivo, which is consistent with the impaired transformed growth observed in PKCe-deficient KRAS-dependent NSCLC cells. Moreover, PKCe-knockout mice were found to be less susceptible to lung tumorigenesis induced by benzo[a]pyrene, a carcinogen that induces mutations in Kras. Mechanistic analysis using RNA-Seq revealed little overlapping for PKCe and KRAS in the control of genes/biological pathways relevant in NSCLC, suggesting that a permissive role of PKCe in KRAS-driven lung tumorigenesis may involve non-redundant mechanisms. Our results thus highlight the relevance and potential of targeting PKCe for lung cancer therapeutics.

2020-07-31 | GSE149205 | GEO

Regulatory T cell depletion promotes oncogenic Kras driven pancreatic tumorigenesis.

Project description:Regulatory T cell depletion promotes oncogenic Kras driven pancreatic tumorigenesis.

| PRJNA492936 | ENA

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Mutant SF3B1 promotes AKT and NF-kB driven mammary tumorigenesis

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The mechanism of elevated S100A6 (Calcyclin) Enhances Tumorigenesis in clear cell renal cell carcinoma

Project description:Among all types of urological cancers, the clear cell renal cell carcinoma is the second leading cause of death in adults. This is mainly due to lack of promising prognosis or predictors, and effective target therapy. S100A6 (calcyclin), a member of S100 family of proteins, is reported to be elevated in many types of cancers. In the present study, we analyzed the expression of S100A6 in mRNA, in proteins and tissues. The mechanism of enhancing tumorigenesis was studied to understand the role of S100A6 in clear cell renal cell carcinoma tumorigenesis. Microarray and bioinformatic analyses were performed in the stable transfection of overexpression and knockdown of S100A6, comparing with each empty vector control in order to find the different expression genes and explore the mechanism. The microarray analysis of clear cell renal cell carcinoma 786-O cell line treated with overexpression and knockdown S100A6. Four samples: overexpression S100A6 sample and vector control sample, knockdown S100A6 and vector control sample, each sample had three replicates.

2013-11-25 | E-GEOD-52708 | biostudies-arrayexpress

Methionine metabolism and the NOP2 methyltransferase are essential for MYC-Driven liver tumorigenesis

Project description:Hepatocellular carcinoma (HCC) represents the third leading cause of cancer-related death worldwide and has been increasing in recent years in developed nations1,2. The MYC oncogene or its paralogs are frequently amplified or overexpressed in particularly aggressive subtypes of cancer associated with stem cell-like features and worse clinical outcomes3,4, including in liver cancer5. Unfortunately, selective inhibitors that target MYC or its transcriptional program are not yet clinically available for therapy of HCC. Here, we identified methionine metabolism as a selective vulnerability for MYC but not RAS-driven liver cancers. MYC-driven liver cancer cells are methionine dependent and S-adenosylmethionine (SAM), the predominant methyl donor, partially rescues methionine depletion. A low methionine diet, or the methylation inhibitor 5-azacytidine limited MYC-driven tumor formation, but RAS-driven liver cancer was resistant to a low methionine diet. Metabolic tracing of methionine catabolism in MYC high cells identified increased m5C methylation of genomic DNA or ribosomal RNA. We identified NOP2, an rRNA m5C-methyltransferase as a MYC target gene. Knockdown of NOP2 selectively inhibited MYC liver cancer cell proliferation and in vivo tumorigenesis. Thus, methionine catabolism is critical for MYC-driven liver tumorigenesis and NOP2 may serve as a new therapeutic target in liver cancer.

2022-10-06 | GSE214724 | GEO

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