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Deficiency of histone methyltransferase SETD2 in liver leads to abnormal lipid metabolism and hepatocarcinoma

ABSTRACT: Deficiency of histone methyltransferase SETD2 in liver leads to abnormal lipid metabolism and hepatocarcinoma

PROVIDER: PRJNA563558 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10059000_1.fastq.gz	Fastqsanger.gz
	SRR10059000_2.fastq.gz	Fastqsanger.gz
	SRR10059200_1.fastq.gz	Fastqsanger.gz
	SRR10059200_2.fastq.gz	Fastqsanger.gz
	SRR10059001_1.fastq.gz	Fastqsanger.gz

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Deficiency of histone methyltransferase SETD2 in liver leads to abnormal lipid metabolism and hepatocarcinoma [RNA-Seq]

Project description:H3K36me3 catalyzed by histone methyltransferase SETD2 is one of the most conserved epigenetic marks from yeast to mammals. SETD2 is frequently mutated in multiple cancers and acts as a tumor suppressor. Here, utilizing a liver-specific deletion of Setd2 mice model, we found that Setd2 depletion is sufficient to trigger hepatocarcinoma (HCC) spontaneously. Meanwhile, in a DEN-induced HCC model, Setd2 depletion significantly promoted tumor number and size. The mechanistic study showed that Setd2 suppresses HCC not only through modulating DNA damage response, but also regulating lipid metabolism in liver. Setd2 deficiency down-regulated the expression of cholesterol efflux genes and caused lipid accumulation. ChIP-Seq analysis further revealed that Setd2 deletion induced AP-1 activation in liver, which was probably trigged by accumulated cholesterol. AP-1 is a well-known oncogene in HCC and inhibits p53 in Setd2-deficient cells. Taken together, we found the role of an important epigenetic gene in regulating cholesterol homeostasis and HCC, and revealed the underlying mechanisms.

2021-09-01 | GSE136742 | GEO

Deficiency of histone methyltransferase SETD2 in liver leads to abnormal lipid metabolism and hepatocarcinoma [ChIP-Seq]

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Deficiency of histone methyltransferase SETD2 in liver leads to abnormal lipid metabolism and hepatocarcinoma [ChIP-Seq]

Project description:Deficiency of histone methyltransferase SETD2 in liver leads to abnormal lipid metabolism and hepatocarcinoma [ChIP-Seq]

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Deficiency of histone methyltransferase SETD2 in liver leads to abnormal lipid metabolism and hepatocarcinoma [RNA-Seq]

Project description:Deficiency of histone methyltransferase SETD2 in liver leads to abnormal lipid metabolism and hepatocarcinoma [RNA-Seq]

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Deficiency of histone methyltransferase SETD2 in liver leads to abnormal lipid metabolism and hepatocarcinoma

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

2021-09-01 | GSE136744 | GEO

SETD2 methyltransferase activity promotes correct transcription initiation and termination

Project description:SETD2 is a methyltransferase responsible for depositing histone H3 lysine 36 trimethylation (H3K36me3). Loss of its enzymatic activity occurs in some cancers, including renal cell carcinoma. SETD2 mutations have been linked to delayed transcription termination, but have not been explored in depth. Here, using nascent transcriptomics in SETD2 knockout and patient-derived cells, we reveal a dichotomy in SETD2 functions depending on the affected protein-coding gene. The majority of genes, named class I, are dependent on SETD2 function for transcription initiation, yet terminate transcription in the usual locations. In contrast, for class II genes, corresponding to 15-25% of active protein-coding genes, transcription initiation is robust in absence of SETD2 activity; however, widespread transcriptional readthrough occurs. Defective termination following SETD2 loss/mutation is associated with increased cryptic transcription initiation and impaired 3′ pre-mRNA cleavage. Additionally, alternative polyadenylation upon SETD2 activity loss is highly cell type specific, and no relationship with transcription readthrough was observed. We demonstrate that methyltransferase activity of SETD2 stimulates proper initiation, prevents cryptic initiation and promotes efficient 3′ end processing, however it does so indirectly.

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SETD2 methyltransferase activity aids gene definition by promoting correct transcription initiation and efficient pre-mRNA 3’ cleavage [U2OS_POINT5]

Project description:SETD2 is a key histone methyltransferase responsible for depositing histone H3 lysine 36 trimethylation (H3K36me3). Loss of its enzymatic activity has been implicated in various cancers, including renal cell carcinoma (RCC). In RCC, SETD2 mutations have been linked to defects in transcription termination, though the underlying mechanism remains unclear. Here, using nascent transcriptomics in SETD2 knockouts and RCC patient-derived cells, we show that SETD2 loss leads to delayed transcription termination, but only in a subset of genes. POINT-seq analysis reveals widespread transcriptional readthrough beyond canonical termination sites upon SETD2 loss/mutation, affecting 15–24% of genes. We demonstrate that defective termination following SETD2 loss/mutation is driven by a combination of increased cryptic transcription initiation and impaired 3′ pre-mRNA cleavage. In contrast, genes that maintain proper termination show significant downregulation. Additionally, we find that SETD2 ensures proper termination independently of alternative polyadenylation, underscoring the distinction between transcription termination and 3′ end processing. Our findings highlight that methyltransferase activity of SETD2 is a crucial regulator of transcriptional integrity, preventing cryptic initiation and promoting efficient 3′ end processing

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