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CSTF2 shortens polyA tail of CXCL10 and drives immune suppression in pancreatic cancer

ABSTRACT: CSTF2 shortens polyA tail of CXCL10 and drives immune suppression in pancreatic cancer

PROVIDER: PRJNA1130860 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29678918_1.fastq.gz	Fastqsanger.gz
	SRR29678918_2.fastq.gz	Fastqsanger.gz
	SRR29678919_1.fastq.gz	Fastqsanger.gz
	SRR29678919_2.fastq.gz	Fastqsanger.gz
	SRR29678920_1.fastq.gz	Fastqsanger.gz

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CSTF2 shortens polyA tail of CXCL10 and drives immune suppression in pancreatic cancer

Project description:Alternative cleavage and polyadenylation (APA) has gained increasing attention in cancer biology, yet its role in tumor immunotherapy resistance remains largely unexplored. Here, we identify the cleavage stimulation factor 2 (CSTF2) in pancreatic ductal adenocarcinoma (PDAC) cells, an APA-related gene, as a novel suppressor of anti-tumor immunity. CSTF2 promotes tumor development by inhibiting the infiltration and function of TCRαβ+CD4–CD8–NK1.1– innate αβ T (iαβT) cells. Mechanistically, CSTF2 downregulates CXCL10 expression by promoting PolyA polymerase alpha (PAPα) binding to the 3' untranslated regions (3'UTR) of CXCL10 RNA, resulting in shortened PolyA tails and reduced RNA stability. Consequently, we identified Forsythoside B, a selective inhibitor of the RNA recognition motif (RRM) of CSTF2, effectively activates anti-tumor immunity and reverses immune checkpoint blockade (ICB) therapy resistance. Collectively, our findings unveil CSTF2 as a promising therapeutic target for sensitizing PDAC to ICB therapy.

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Determination of transcript's polyA tail length in Wild-Type and Mov10 KO mouse ESCs.

Project description:The RNA helicase MOV10 targets mRNAs to promote their decay. MOV10 can directly bind to N6-methyladenosine (m6A) nucleotides, the most prevalent type of mRNA internal modification in mammals. Here we investigate the mechanism by which MOV10 promotes decay by looking at changes in the polyA tail of its targets. PolyA tail length shortening is usually associated with transcript decay. However, we did not observe changes in the polyA profile for MOV10 targets in MOV10-depleted and Wild-Type controls. The observation was true for targeted transcripts containing the m6A modification and for targeted transcripts without the modification. We conclude that MOV10-mediated decay does not perturb the polyA tail dynamics of its targets in ESCs.

2021-08-26 | GSE181746 | GEO

Project description:The role and mechanism of CSTF2 in hepatocellular carcinoma are unclear. We constructed CSTF2 knockout HUH7 and PLC/PRF/5 cells to analyze the function of CSTF2 in liver cancer and the downstream gene changes it induces.

2024-02-10 | GSE254649 | GEO

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Project description:CSTF2, an RNA-binding protein, and its target genes in hepatocellular carcinoma remain unreported. Screening for potential CSTF2-bound RNA sequences was performed using RIP-seq technique in HUH7 cells.

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MeRIP-seq analysis for CSTF2 knockout in HUH7 and PLC/PRF/5 cell lines

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Determination of transcript's polyA tail length in Wild-Type and Mov10 KO mouse ESCs.

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