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CRKL regulates alternative splicing of genes that function in tumorigenesis and cancer progression

ABSTRACT: CRKL regulates alternative splicing of genes that function in tumorigenesis and cancer progression

PROVIDER: PRJNA495833 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8032921_1.fastq.gz	Fastqsanger.gz
	SRR8032921_2.fastq.gz	Fastqsanger.gz
	SRR8032922_1.fastq.gz	Fastqsanger.gz
	SRR8032922_2.fastq.gz	Fastqsanger.gz
	SRR8032923_1.fastq.gz	Fastqsanger.gz

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CRKL regulates alternative splicing of genes that function in tumorigenesis and cancer progression

Project description:CRKL adaptor protein was demonstrated to have important effects in various types of human cancer and contributes to malignant cell growth and chemoresistance as an overexpressed oncoprotein in cervical carcinoma. But the special molecular mechanisms of CRKL in cervical cancer remain unknown. Here we reported that CRKL regulates genes in cervical cancer related pathways via targeting alternative splicing. We analyzed the expression level of CRKL in 300 cervical cancer tissue samples available in TCGA database, showing a significant increase expression in Stage I cancer samples. From these tumor samples, we selected 40 cancer samples with 20 showing high CRKL expression and 20 showing low, which were analyzed for the potential impact of CRKL on alternative splicing regulation of cancer transcriptome. We further explored the potential function of CRKL in promoting cell proliferation and regulating alternative splicing in HeLa cells using shRNA to knock-down CRKL expression. More importantly, we showed that 34 (94%) of CRKL-regulated alternative splicing events detected in HeLa cells could be validated by qPCR approach and more than a half of these validated events detected in HeLa cells were also correlated with the CRKL expression level in cervical cancers. These results together support a conclusion that CRKL adaptor protein extensively regulates alternative splicing of many genes which are important in tumorigenesis and cancer progression, which expands the functional importance of signaling adaptors in coordinating the dynamic activation of signaling pathways with cellular responses at the alternative splicing level.

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SAM68 promotes Lung adenocarcinoma tumorigenesis by regulating cancer metabolic conversion through alternative splicing

Project description:The metabolic conversion of oxidative phosphorylation to glycolysis provides tumor cells with energy and biosynthetic substrates, thereby promoting tumorigenesis and malignant progression. However, the mechanisms controlling the tumor metabolic switch is still not entirely clear. Here we demonstrate that SAM68 (gene name: KHDRBS1) as a splicing regulatory factor is frequently overexpressed in Lung adenocarcinoma (LUAD) and negatively correlated with the prognosis of LUAD patients. we find SAM68 promotes LUAD cells tumorigenesis and metastasis both in vitro and in vivo by regulating cancer metabolic switch. SAM68 drives cancer metabolism by mediating alternative splicing of Pyruvate kinase (PKM) pre-mRNAs, finally promoting the formation of PKM2. Mechanically, Sam68 interacted with the splicing repressor hnRNP A1, and depletion of hnRNP A1 or mutations that impair this interaction attenuated the PKM splicing regulation. Together, our work demonstrates key roles of SAM68 in the cancer metabolic conversion by regulating alternative splicing and SAM68 may be a promising therapeutic target for treating LUAD.This project looks into how SAM68 levels affect cancer cell phenotype in vitro

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DIS3L2 promotes progression of hepatocellular carcinoma via hnRNP U-mediated alternative splicing

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