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Study on differentially expressed genes in the WT1 overexpressed group and the control group by RNA-seq

ABSTRACT: Study on differentially expressed genes in the WT1 overexpressed group and the control group by RNA-seq

PROVIDER: PRJNA598831 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10822467.fastq.gz	Fastqsanger.gz
	SRR10822468.fastq.gz	Fastqsanger.gz
	SRR10822469.fastq.gz	Fastqsanger.gz
	SRR10822470.fastq.gz	Fastqsanger.gz
	SRR10822471.fastq.gz	Fastqsanger.gz

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Study on differentially expressed genes in the WT1 overexpressed group and the control group by RNA-seq

Project description:Purpose: The aim was to find the differentially expressed genes between the WT1 overexpressed group and the control group Methods:Hacat cell was transfected with WT1 overexpressed plasmids and blank plasmids, then RNA from both groups of cells was sequenced. The data obtained from the sequencing is called raw reads, and then the raw reads are subject to quality control QC. After the quality control is passed, the filtered clean reads are compared to the reference genome, This was followed by gene Quantitative analysis, gene expression level based analyses, and more in depth mining analyses such as GO functional significance enrichment analysis and pathway significance enrichment analysis for the selected differentially expressed genes between samples. Conclusions:Our study was the first to analyze the transcriptome of Hacat cells overexpressing WT1 generated by RNA-seq technique and to conduct biological replication. Six samples were measured using BGISEQ-500 platform, and the average output of each sample was 21.89 m. The average ratio of sample to genome was 94.81% . A total of 17,693 genes were detected. A total of 181 differentially expressed genes between the two groups were analyzed by GO and Kegg.

2023-01-03 | GSE142985 | GEO

Transcription profiling of human WT1-mutant versus WT1 wild-type Wilms tumors

Project description:Gain-of-function mutations in exon 3 of beta-catenin (CTNNB1) are specific for Wilms' tumors that have lost WT1, but 50% of WT1-mutant cases lack such "hot spot" mutations. To ask whether stabilization of beta-catenin might be essential after WT1 loss, and to identify downstream target genes, we compared expression profiles in WT1-mutant versus WT1 wild-type Wilms' tumors. Supervised and nonsupervised hierarchical clustering of the expression data separated these two classes of Wilms' tumor. The WT1-mutant tumors overexpressed genes encoding myogenic and other transcription factors (MOX2, LBX1, SIM2), signaling molecules (TGFB2, FST, BMP2A), extracellular Wnt inhibitors (WIF1, SFRP4), and known beta-catenin/TCF targets (FST, CSPG2, CMYC). Beta-Catenin/TCF target genes were overexpressed in the WT1-mutant tumors even in the absence of CTNNB1 exon 3 mutations, and complete sequencing revealed gain-of-function mutations elsewhere in the CTNNB1 gene in some of these tumors, increasing the overall mutation frequency to 75%. Lastly, we identified and validated a novel direct beta-catenin target gene, GAD1, among the WT1-mutant signature genes. These data highlight two molecular classes of Wilms' tumor, and indicate strong selection for stabilization of beta-catenin in the WT1-mutant class. Beta-Catenin stabilization can initiate tumorigenesis in other systems, and this mechanism is likely critical in tumor formation after loss of WT1. Experiment Overall Design: Identification of WNT/Beta-Catenin or WT1 target genes. 39 individual samples.

2008-06-14 | E-GEOD-6120 | biostudies-arrayexpress

Differentially expressed genes following ARID1A depletion

Project description:Differentially expressed genes following ARID1A depletion

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Differentially expressed miRNAs in colorectal cancer

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Effect of the silencing of WT1 expression on HCC transcriptome

Project description:The Wilms´ tumor 1 gene (WT1) encodes a transcription factor involved in cell growth and development. As we previously reported WT1 expression is hardly detectable in normal hepatic tissue but is induced in liver cirrhosis. Although WT1 has been found to be overexpressed in a number of malignancies, the role of WT1 in hepatocarcinogenesis has not been clarified. We found that WT1 is expressed in several human hepatocellular carcinoma (HCC) cell lines including PLC/PRF/5 and HepG2, and in HCC tumor tissue in 42% of patients. WT1 small interfering RNAs did not affect proliferation rate of HCC cells but abrogated their resistance to anoikis. Transcriptome analysis of PLC/PRF/5 cells after WT1 knockdown demonstrated upregulation of 251 genes and downregulation of 321. Ninety per cent of the former corresponded to metabolic genes mostly those characterizing the mature hepatocyte phenotype. On the contrary, genes that decreased upon WT1 inhibition were mainly related to defense against apoptosis, cell cycle and tumor progression. In agreement with these findings WT1 expression increased the resistance of liver tumor cells to doxorubicin, a compound used to treat HCC. Interestingly, doxorubicin strongly enhanced WT1 expression in both HCC cells and normal human hepatocytes. Among different chemotherapeutics, induction of WT1 transcription was restricted to topoisomerase 2 inhibitors. When WT1 expression was prohibited doxorubicin caused a marked increase in caspase-3 activation. In conclusion, WT1 is expressed in a substantial proportion of HCC contributing to tumor progression and resistance to chemotherapy, suggesting that WT1 may be an important target for HCC treatment. Keywords: Cell type comparison

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