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The LINC01138 Drives Malignancies via Activating Arginine Methyltransferase 5 in Hepatocellular Carcinoma

ABSTRACT: The LINC01138 Drives Malignancies via Activating Arginine Methyltransferase 5 in Hepatocellular Carcinoma

PROVIDER: PRJNA437713 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6823460.fastq.gz	Fastqsanger.gz
	SRR6823455_1.fastq.gz	Fastqsanger.gz
	SRR6823455_2.fastq.gz	Fastqsanger.gz
	SRR6823456_1.fastq.gz	Fastqsanger.gz
	SRR6823456_2.fastq.gz	Fastqsanger.gz

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The LINC01138 Drives Malignancies via Activating Arginine Methyltransferase 5 in Hepatocellular Carcinoma

Project description:Our study have demonstrated LINC01138 acts as an oncogenic driver that promotes cell proliferation, tumourigenicity, tumour invasion and metastasis through physically interacting with Arginine Methyltransferase 5 (PRMT5) in HCC cells. In order to investigate the related signaling pathways regulated by LINC01138 or PRMT5, we performed the unbiased transcriptome profiling using high-throughput RNA sequencing in SMMC-7721 cells transfected with si-LINC01138 or si-PRMT5. Here we showed the LINC01138/PRMT5 axis is an ideal therapeutic target for HCC treatment.

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The LINC01138 drives malignancies via activating arginine methyltransferase 5 in hepatocellular carcinoma.

Project description:Recurrent chromosomal aberrations have led to the discovery of oncogenes or tumour suppressors involved in carcinogenesis. Here we characterized an oncogenic long intergenic non-coding RNA in the frequent DNA-gain regions in hepatocellular carcinoma (HCC), LINC01138 (long intergenic non-coding RNA located on 1q21.2). The LINC01138 locus is frequently amplified in HCC; the LINC01138 transcript is stabilized by insulin like growth factor-2 mRNA-binding proteins 1/3 (IGF2BP1/IGF2BP3) and is associated with the malignant features and poor outcomes of HCC patients. LINC01138 acts as an oncogenic driver that promotes cell proliferation, tumorigenicity, tumour invasion and metastasis by physically interacting with arginine methyltransferase 5 (PRMT5) and enhancing its protein stability by blocking ubiquitin/proteasome-dependent degradation in HCC. The discovery of LINC01138, a promising prognostic indicator, provides insight into the molecular pathogenesis of HCC, and the LINC01138/PRMT5 axis is an ideal therapeutic target for HCC treatment.

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