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EYA4 is a non-small cell lung cancer tumor suppressor located in the susceptibility locus on chromosome 6q

ABSTRACT: This study was undertaken to identify novel tumour suppressor genes in lung adenocarcinoma. EYA4, located at 6q23.2 was identified as a frequently lost and hypermethylated gene in the analyzed samples. EYA4 is underexpressed in addition to being deleted and hypermethylated. Control of EYA4 expression by DNA methylation was assessed using 5'-azacytidine. The role of EYA4 in apoptosis was assessed using a stable knock down of the gene which was assessed for apoptotis using FACS and qPCR.

ORGANISM(S): Homo sapiens

PROVIDER: GSE19034 | GEO | 2014/02/25

SECONDARY ACCESSION(S): PRJNA120637

REPOSITORIES: GEO

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EYA4 is a non-small cell lung cancer tumor suppressor located in the susceptibility locus on chromosome 6q

Project description:This study was undertaken to identify novel tumour suppressor genes in lung adenocarcinoma. EYA4, located at 6q23.2 was identified as a frequently lost and hypermethylated gene in the analyzed samples. EYA4 is underexpressed in addition to being deleted and hypermethylated. Control of EYA4 expression by DNA methylation was assessed using 5'-azacytidine. The role of EYA4 in apoptosis was assessed using a stable knock down of the gene which was assessed for apoptotis using FACS and qPCR. Methylation profiling: 30 adenocarcinoma samples and 30 patient-matched non-malignant lung samples are included. Non-malignant samples were used as references to identify hypermethylated probes. For each normal/tumor pair, the sample numbers are paired but offset by one with the tumor being the lower of the two numbers. For example, 85040001 is the adenocarcinoma tumor profile that pairs with non-malignant 85040002. Genome variation (aCGH) profiling: 30 adenocarcinoma gene dosage profiles are included. Values presented are log2 ratios of Cy3(sample)/Cy5(diploid reference)

2014-02-25 | E-GEOD-19034 | biostudies-arrayexpress

An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer: CGH

2010-12-31 | GSE21540 | GEO

An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer: CGH

Project description:This study was undertaken to identify novel tumour suppressor genes in lung adenocarcinoma. EYA4, located at 6q23.2 was identified as a frequently lost and hypermethylated gene in the analyzed samples. 7 Breast cancer cell lines profiled on the SMRTr array in conjunction with matched DNA methylation data, allelic status and gene expression data for integrative analysis.

2010-12-31 | E-GEOD-21540 | biostudies-arrayexpress

Novel cleft susceptibility genes in chromosome 6q.

Project description: Not available

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LC-MSMS of the MHC-I immunopeptidome of AML cell lines

Project description:The hypomethylating agent 5-azacytidine (AZA) is the first-line induction therapy for AML patients unsuitable for intensive chemotherapy. The anti-tumor effect of AZA results in part from T-cell cytotoxic responses against MHC-I-associated peptides (MAPs) deriving from hypermethylated genomic regions such as cancer-testis antigens (CTAs), or endogenous retroelements (EREs). However, clear evidence supporting higher ERE MAPs presentation after AZA treatment in AML is lacking. Therefore, we examined the immunopeptidome of four AML cell lines treated with AZA through a proteogenomic approach to validate this hypothesis.

2024-04-17 | PXD038663 | Pride

Temporal resolution of gene derepression and proteome changes upon PROTAC-mediated degradation of BCL11A protein in erythroid cells [DNA methylation]

Project description:We acutely depleted the BCL11A protein by using the dTAG PROTAC technology, and assessed its immediate consequences on DNA methylation, in the presence/absence of DNMT1 inhibitor AZAcytidine.

2022-07-19 | GSE194340 | GEO

DNA Methyltransferase inhibition reverses epigenetically embedded phenotypes in lung cancer preferentially affecting Polycomb target genes

Project description:Cancer cell phenotypes are partially determined by epigenetic specifications such as DNA methylation. Metastasis development is a late event in cancerogenesis and might be associated with epigenetic alterations. Here, we analyzed genome wide DNA methylation changes that were associated with pro-metastatic phenotypes in non-small cell lung cancer with Reduced Representation Bisulfite Sequencing. DNMT-inhibition by 5-Azacytidine at low concentrations reverted the pro-metastatic phenotype. 5-Azacytidine led to preferential loss of DNA methylation at sites that were DNA hypermethylated during the in vivo selection. Changes in DNA methylation persisted over time. Refer to individual Series

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DNA Methyltransferase inhibition reverses epigenetically embedded phenotypes in lung cancer preferentially affecting Polycomb target genes

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RNAseq to investigate transcriptional changes in human MM cell lines due to panobinostat, 5-Azacytidine, panobinostat+5-Azacytidine or n-methyl-2-pyrroldine (NMP) treatments.

Project description:Purpose: We applied RNA sequencing technology for high-throughput analysis of transcriptional changes within human MM cell lines JJN3 and U266 due to individual and combination drug treatment. Methods: JJN3 and U266 cells were treated with pan-HDACi panbobinostat, DNMTi 5-Azacytidine, panobinostat+5-Azacytidine or NMP for 4h or 24h in triplicate and transcriptional changes assessed by RNAseq using Illumina HiSeq platform. Specifically, JJN3 cells were treated with 10nM panobinostat, 2.5µM 5-Azacytidine, panobinostat+5-Azacytidine (at given doses), or 10mM NMP. U266 cells were treated with 10nM panobinostat, 10µM 5-Azacytidine, panobinostat+5-Azacytidine (at given doses), or 10mM NMP. Results: We report unique and overlapping transcriptional signatures that lead to the induction of apoptosis in human MM cell lines in a cell-specific manner due to individual or combination treatments. Conclusions: A detailed analysis of differential transcriptional events in human MM cell lines due to HDACi, DNMTi, HDACi+DNMTi and NMP appear to define the molecular events leading to apoptosis and drug mechanism of action.

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Project description:The hypomethylating agent 5-azacytidine (AZA) is the first-line induction therapy for AML patients unsuitable for intensive chemotherapy. The anti-tumor effect of AZA results in part from T-cell cytotoxic responses against MHC-I-associated peptides (MAPs) deriving from hypermethylated genomic regions such as cancer-testis antigens (CTAs), or endogenous retroelements (EREs). However, clear evidence supporting higher ERE MAPs presentation after AZA treatment in AML is lacking. Interestingly, we find that AZA-mediated DNMT2 inhibition leads to autophagy induction, which is responsible for mitigating ERE MAPs generation. To validate our findings, we examined the immunopeptidome of THP-1 cells treated with AZA combined with autophagy inhibitor, Spautin-1 or decitabine (DAC, non-DNMT2 inhibiting HMA) through a proteogenomic approach.

2024-04-17 | PXD046853 | Pride

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