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The epithelial splicing regulator ESRP2 is epigenetically repressed by DNA hypermethylation in Wilms tumor and acts as a tumor suppressor

ABSTRACT: The epithelial splicing regulator ESRP2 is epigenetically repressed by DNA hypermethylation in Wilms tumor and acts as a tumor suppressor

PROVIDER: PRJNA646492 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12229281_1.fastq.gz	Fastqsanger.gz
	SRR12229281_2.fastq.gz	Fastqsanger.gz
	SRR12229282_1.fastq.gz	Fastqsanger.gz
	SRR12229282_2.fastq.gz	Fastqsanger.gz
	SRR12229283_1.fastq.gz	Fastqsanger.gz

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The epithelial splicing regulator ESRP2 is epigenetically repressed by DNA hypermethylation in Wilms tumor and acts as a tumor suppressor

Project description:Wilms tumor (WT), a childhood kidney cancer with embryonal origins, has been extensively characterised for genetic and epigenetic alterations, but a proportion of WTs still lack identifiable abnormalities. To uncover DNA methylation changes critical for WT pathogenesis, we compared the epigenome of fetal kidney with two WT cell lines, using methyl-CpG immunoprecipitation. We filtered our results to remove common cancer-associated epigenetic changes, and to enrich for genes involved in early kidney development. This identified four candidate genes that were hypermethylated in WT cell lines compared to fetal kidney, of which ESRP2 (epithelial splicing regulatory protein 2), was the most promising gene for further study. ESRP2 was commonly repressed by DNA methylation early in WT development (in nephrogenic rests) and could be reactivated by DNA methyltransferase inhibition in WT cell lines. When ESRP2 was expressed in WT cell lines, it acted as an inhibitor of cellular proliferation in vitro and in vivo it suppressed tumor growth of orthotopic xenografts in nude mice. RNA-seq of the ESRP2-expressing WT cell lines identified several novel splicing targets, in addition to well-characterised targets of ESRP2. One of these targets, LEF1, is a component of the Wnt signalling pathway that is essential for kidney development and commonly disrupted in WT. We propose a model in which the Wnt pathway can be disrupted in early kidney development to generate WT, either by genetic abnormalities such as WT1 mutations, or by epigenetic defects, such as ESRP2 methylation.

2020-11-02 | GSE154496 | GEO

The epithelial splicing regulator ESRP2 is epigenetically repressed by DNA hypermethylation in Wilms tumour and acts as a tumour suppressor

Project description:Wilms tumour (WT), a childhood kidney cancer with embryonal origins, has been extensively characterised for genetic and epigenetic alterations, but a proportion of WTs still lack identifiable abnormalities. To uncover DNA methylation changes critical for WT pathogenesis, we compared the epigenome of fetal kidney with two WT cell lines, using methyl-CpG immunoprecipitation. We filtered our results to remove common cancer-associated epigenetic changes, and to enrich for genes involved in early kidney development. This identified four candidate genes that were hypermethylated in WT cell lines compared to fetal kidney, of which ESRP2 (epithelial splicing regulatory protein 2), was the most promising gene for further study. ESRP2 was commonly repressed by DNA methylation early in WT development (in nephrogenic rests) and could be reactivated by DNA methyltransferase inhibition in WT cell lines. When ESRP2 was expressed in WT cell lines, it acted as an inhibitor of cellular proliferation in vitro and in vivo it suppressed tumour growth of orthotopic xenografts in nude mice. RNA-seq of the ESRP2-expressing WT cell lines identified several novel splicing targets, in addition to well-characterised targets of ESRP2. One of these targets, LEF1, is a component of the Wnt signalling pathway that is essential for kidney development and commonly disrupted in WT. We propose a model in which the Wnt pathway can be disrupted in early kidney development to generate WT, either by genetic abnormalities such as WT1 mutations, or by epigenetic defects, such as ESRP2 methylation. The microarray data in this deposition identified ESRP2 as a commonly hypermethylated gene in Wilms tumour.

2020-11-02 | GSE153047 | GEO

The epithelial splicing regulator ESRP2 is epigenetically repressed by DNA hypermethylation in Wilms tumour and acts as a tumour suppressor

Project description:The epithelial splicing regulator ESRP2 is epigenetically repressed by DNA hypermethylation in Wilms tumour and acts as a tumour suppressor

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miRNA and Wilms' tumor

Project description:miRNA and Wilms' tumor

| PRJNA139175 | ENA

Sequencing-based analyses characterize a tumor suppressive role of mir-1271 repressed by DNA hypermethylation in gastric cancer

Project description:To identify tumor suppressive microRNAs repressed by DNA hypermethylation in gastric cancer (GC), we analyzed methylome and miRNome of EpCAM+/CD44+ GC cells. Among a set of microRNAs hypermethylated and downregulated in GC, mir-1271 was uncovered as a microRNA repressed by DNA hypermethylation in GC. Forced expression of mir-1271 significantly suppressed growth, migration, and invasion of GC cells both in vitro and in vivo. To identify target genes and cancer signaling pathways regulated by mir-1271, we examined differentially-expressed genes responsive to mir-1271 by performing RNA-sequencing.

2018-06-12 | GSE87785 | GEO

Transcriptomic Characterization of wilms tumor

Project description:Wilms tumor (WT) is the most common renal malignancy in children. So we aim to investigate the transcriptomic map of Wilms tumor.

2022-05-18 | GSE138869 | GEO

Transcriptomic Characterization of wilms tumor

Project description:Transcriptomic Characterization of wilms tumor

| PRJNA577648 | ENA

miRNA and Wilms' tumor

Project description:This SuperSeries is composed of the following subset Series: GSE17342: The role of miRNA in Wilms' tumorigenesis GSE28397: Copy number alteration in Wilms' tumor with custom-designed miRNA probes GSE28400: MIR-204 target gene Refer to individual Series

2012-03-30 | E-GEOD-28401 | biostudies-arrayexpress

Circulating miRNA in serum of Wilms tumor patients

Project description:Abstract: Background: MiRNA signatures in human sera have been reported for various tumor diseases. Here we generated miRNA profiles analyzing 1205 mature miRNA transcripts of serum samples of Wilms tumor patients, taken prior and after chemotherapy according to SIOP protocol 2001. Using a feature subset selection filter approach we identified a minimal number of miRNAs with a maximum contribution for the classification between treated and untreated patients and between patients and controls. Results: Analyzing 1205 mature miRNAs, we separated controls and Wilms tumor patients prior chemotherapy with an accuracy of 0.81. We obtained a similar accuracy (0.82) for the separation between controls and sera of Wilms tumor patients after preoperative chemotherapy. We identified 23 miRNAs that were differentially expressed in both comparisons. Subset selection improved the overall classification accuracy between controls and Wilms tumor patients prior and after chemotherapy to 0.94 and 0.91, respectively. Subset selection also allowed separating between Wilms tumor patients prior and after chemotherapy with an accuracy of 0.98. Conclusion: Our analysis identified serum based miRNA signatures that allowed separating between controls, untreated Wilms tumor patients, and Wilms tumor patients after chemotherapy with high accuracy for each of these comparisons.

2014-12-31 | GSE48137 | GEO

Proteasome inhibition sensitizes anaplastic Wilms tumor to actinomycin D

Project description:Wilms tumor is the most common kidney cancer in children, and anaplastic Wilms tumor is the most chemoresistant histological subtype. Here we explore how anaplastic Wilms tumor cells evade the common chemotherapeutic drug actinomycin D, which inhibits ribosomal biogenesis. We found that, when ribosomal capacity is limited by actinomycin D treatment, anaplastic Wilms tumor cells preferentially translate proteasome components and upregulate proteasome activity. Accordingly, increased proteasome levels are associated with anaplastic histology and with worse prognosis in Wilms tumor. Lastly, we show that the proteasome inhibitor bortezomib sensitizes cells to actinomycin D treatment both in vitro and in vivo.

2024-06-20 | GSE270330 | GEO

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