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Effect of depletion of NUDT21 on gene expression in HCT116

ABSTRACT: Effect of depletion of NUDT21 on gene expression in HCT116

PROVIDER: PRJNA926109 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23176566_1.fastq.gz	Fastqsanger.gz
	SRR23176566_2.fastq.gz	Fastqsanger.gz
	SRR23176567_1.fastq.gz	Fastqsanger.gz
	SRR23176567_2.fastq.gz	Fastqsanger.gz
	SRR23176568_1.fastq.gz	Fastqsanger.gz

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Effect of depletion of NUDT21 on gene expression in HCT116

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NUDT21 alters glioma migration through differential alternative polyadenylation of LAMC1

Project description:We identified LAMC1 as a critical NUDT21 target involved in several core glioma-driving signaling pathways. qRT-PCR analysis confirmed that NUDT21-knockdown in GBM cells resulted in the preferred usage of the proximal C/PAS of LAMC1. Furthermore, functional studies revealed that NUDT21-knockdown-induced 3’UTR shortening of LAMC1 was sufficient to induce translational gain, as LAMC1 was upregulated in these cells compared to their respective controls. Additionally, we demonstrated that primary glial cells recapitulated this phenomenon. We also further dissected the miRNA-mediated mechanism by which LAMC1 expression was regulated by showing that NUDT21 knockdown in glioma cells directed the 3’UTR shortening of LAMC1, removing binding sites for miR-124/506 and consequently inducing LAMC1 expression. Remarkably, we reported that the knockdown of NUDT21 significantly promoted GBM cell migration and that co-depletion of LAMC1 and NUDT21 abrogated this effect. Lastly, we observed that LAMC1 3’UTR shortening predicted poor prognosis of low- and high-grade glioma patients from The Cancer Genome Atlas.

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NUDT21 Negatively Regulates PSMB2 and CXXC5 by Alternative Polyadenylation and Contributes to Hepatocellular Carcinoma Suppression

Project description:HCC is the third leading cause of cancer-related deaths worldwide. However, the molecular mechanisms underlying the progression of HCC is still largely elusive. NUDT21 (CFIm25) is an important mediator of 3′ UTR APA and demonstrates a causal relationship between alternative polyadenylation and cancer cell proliferation. Although the function of NUDT21 has been explored in glioblastoma tumor, the functional significance of NUDT21 in solid tumors is not well understood. In this study, we observed that NUDT21 is suppressed in human HCC tissues, compared to adjacent noncancerous tissues. In addition we found that the HCC patients with suppressed NUDT21 are statistically associated with poor outcomes. These observations suggest NUDT21 possibly functions as tumor suppressor in hepatocellular carcinoma (HCC).

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NUDT21 regulates intron detention of the SAM synthetase MAT2A RNA

Project description:NUDT21 encodes the CFIm25 protein, a component of the CFIm complex that regulates alternative polyadenylation (APA). Our data suggest that the CFIm complex also induces splicing of a detained intron in the the S-adenosylmethionine (SAM) synthetase MAT2A to control intracellular levels of SAM. To genetically separate these functions, we used poly(A) Click-seq (PAC-seq) to determine the changes in poly(A) site selection in two cell lines. The parental cell line is the colorectal cell line HCT116 and a derivative line that has the detained intron of MAT2A deleted in both alleles of MAT2A (116-DDI). We found few differences in alternative polyadenylation after CFIm25 depletion were similar supporting teh conclusion that CFIm's role in APA is mechanistically distinct from its role in regulation of MATA splicing.

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