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Transcriptome changes after knocking out MYEOV in two human pancreatic cancer cell lines

ABSTRACT: Transcriptome changes after knocking out MYEOV in two human pancreatic cancer cell lines

PROVIDER: PRJNA601781 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10905104_1.fastq.gz	Fastqsanger.gz
	SRR10905104_2.fastq.gz	Fastqsanger.gz
	SRR10905105_1.fastq.gz	Fastqsanger.gz
	SRR10905105_2.fastq.gz	Fastqsanger.gz
	SRR10905106_1.fastq.gz	Fastqsanger.gz

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microRNA expression changes after knocking out MYEOV in two human pancreatic cancer cell lines

Project description:microRNA expression changes after knocking out MYEOV in two human pancreatic cancer cell lines

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Transcriptome changes after knocking out MYEOV in two human pancreatic cancer cell lines

Project description:Pancreatic cancer (PC) remains a highly lethal malignancy worldwide. As metastasis and malignant proliferation are primarily responsible for poor clinical outcomes of PC, it is imminent to dig out the pivotal gene involved in the process as well as its underlying molecular mechanism. In this study, through analysis of TCGA and GTEx data, we found that the expression level of MYEOV was obviously increased in carcinoma tissues relative to healthy ones and associated with poor survival in PC patients. The elevated abundance of MYEOV was positively correlated with enhanced cell proliferation, invasion and migration in vivo and in vitro. The global transcriptome analysis of MYEOV-depleted PC cells revealed the downregulation of various genes involved in active cell proliferation, which indicated that MYEOV overexpression was critical for PC progression. MiRNA-seq analysis showed that MYEOV had a regulatory effect on the expression levels of miR-17-5p and miR-93-5p, depletion of which resulted in reduced cell proliferation, invasion and migration as observed in MYEOV-knockdown PC cells. Such effect was imposed by MYEOV through affecting enrichment of the transcription factor c-myc at the gene promoter regions of the two miRNAs. Furthermore, a complex containing MYEOV and MYC was confirmed to exist in cell nucleus, providing convictive evidence for the association of MYEOV with MYC. Together, these results suggested that the axis of MYEOV-MYC-miR-17/93-5p could be vital for PC progression and could act as a potential therapeutic target to interrupt cell proliferation which will benefit treatment and management of PC patients.

2022-01-01 | GSE143827 | GEO

microRNA expression changes after knocking out MYEOV in two human pancreatic cancer cell lines

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Effect of knocking out SOCS3 in mouse ES cells

Project description:Series contains four arrays - two wildtype, two null. The experiment studied the effect of knocking out SOCS3 in mouse ES cells. Keywords: other

2005-02-02 | GSE2202 | GEO

Transcriptional changes induced by ADH5 knocking out in HeLa cells.

Project description:Transcriptional changes induced by ADH5 knocking out in HeLa cells.

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Transcriptome measurements after knocking out the UMLILO lncRNA

Project description:Transcriptome measurements after knocking out the UMLILO lncRNA

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Effect of knocking out RNVU1-18 on gene expression

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Transcriptome measurements after knocking out the UMLILO lncRNA

Project description:Purpose: Assess whether knocking out the UMLILO lncRNA altered the expression of genes transcribed within the CXCL chemokine TAD Outcome: To confirm whether the effect of UMLILO was limited to the CXCL TAD. Adeno-associated viral vectors (AAVs) were constructed that contain CRISPR/Cas9 and guides targeting UMLILO to delete the full length UMLILO transcript. RNAseq was performed on a transduced THP-1 population to verify genome-wide effects of UMLILO depletion. This revealed that IL8, CXCL1, 2, 3 transcription was abrogated, but a similar effect was not seen for genes located outside of the CXCL TAD boundary

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Project description:Chimeric antigen receptor modified T (CAR-T) cell therapy has limited efficacy against solid tumor, one major challenge is T cell exhaustion. To address this challenge, we performed a candidate gene screen using a hypofunction CAR-T cell model, and found that knocking out BATF improved the performance of CAR-T cells. In different types of CAR-T cells and mouse OT-1 cells, knocking out BATF endows T cells with improved resistance to exhaustion and better tumor eradication efficacy. We find that BATF binds to and up-regulates a subset of exhaustion genes in human CAR-T cells. Furthermore, BATF regulates the expression of genes involved in the development of effector and memory cells, and knocking out BATF shifts the population towards more central memory subset. Therefore, we conclude that BATF is a key factor limiting CAR-T cell function, and its depletion improves CAR-T cells efficacy against solid tumor.

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