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Transcription factor ZNF263 enhances EGFR-targeted therapeutic response and reduces residual disease in lung adenocarcinoma [ChIP-seq]

ABSTRACT: Transcription factor ZNF263 enhances EGFR-targeted therapeutic response and reduces residual disease in lung adenocarcinoma [ChIP-seq]

PROVIDER: PRJNA1066855 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27652925_1.fastq.gz	Fastqsanger.gz
	SRR27652925_2.fastq.gz	Fastqsanger.gz
	SRR27652926_1.fastq.gz	Fastqsanger.gz
	SRR27652926_2.fastq.gz	Fastqsanger.gz
	SRR27652927_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Transcription factor ZNF263 enhances EGFR-targeted therapeutic response and reduces residual disease in lung adenocarcinoma [RNAseq2]

Project description:EGF receptor (EGFR) tyrosine kinase inhibitors (TKIs) have achieved clinical successes in lung adenocarcinoma (LUAD). However, tumors often show profound but transient initial response and gain resistance. Here, we identified transcription factor ZNF263 as being significantly decreased in osimertinib-resistant or drug-tolerant persister LUAD cells and clinical residual tumor specimens. Exogenous expression of ZNF263 improved the initial response of cells and delayed the formation of persister cells with osimertinib. We elaborated that ZNF263 bound and recruited DNMT1 to the EGFR gene promoter, suppressing EGFR transcription with DNA hypermethylation. ZNF263 could also interact with nuclear EGFR (nEGFR), impairing the nEGFR-STAT5 interaction to enhance AURKA expression. Overexpressing ZNF263 also made tumor cells with wild-type EGFR expression or refractory EGFR mutations more susceptible to EGFR inhibition. More importantly, lentivirus or AAV-mediated plasmid delivery of ZNF263 synergistically suppressed tumor growth and regrowth with osimertinib in xenograft animal models. These findings suggest that enhancing ZNF263 may achieve complete response in LUAD with EGFR-targeted therapies.

2024-01-23 | GSE253742 | GEO

Transcription factor ZNF263 enhances EGFR-targeted therapeutic response and reduces residual disease in lung adenocarcinoma [RNAseq]

2024-01-23 | GSE253741 | GEO

Transcription factor ZNF263 enhances EGFR-targeted therapeutic response and reduces residual disease in lung adenocarcinoma [ChIP-seq]

2024-01-23 | GSE253745 | GEO

Transcription factor ZNF263 enhances EGFR-targeted therapeutic response and reduces residual disease in lung adenocarcinoma [RNAseq]

Project description:Transcription factor ZNF263 enhances EGFR-targeted therapeutic response and reduces residual disease in lung adenocarcinoma [RNAseq]

| PRJNA1066852 | ENA

Transcription factor ZNF263 enhances EGFR-targeted therapeutic response and reduces residual disease in lung adenocarcinoma [RNAseq2]

Project description:Transcription factor ZNF263 enhances EGFR-targeted therapeutic response and reduces residual disease in lung adenocarcinoma [RNAseq2]

| PRJNA1066854 | ENA

Transcription factor ZNF263 enhances EGFR-targeted therapeutic response and reduces residual disease in lung adenocarcinoma

Project description:CoIP-based mass spectrometry data of ZNF263 binding proteins

2024-01-16 | PXD048574 |

Genomic targets of the KRAB and scan domain-containing zinc finger protein 263 (ZNF263).

Project description:Half of all human transcription factors use C2H2 zinc finger domains to specify site-specific DNA binding and yet very little is known about their role in gene regulation. Based on in vitro studies, a zinc finger code has been developed that predicts a binding motif for a particular zinc finger factor (ZNF). However, very few studies have performed genome-wide analyses of ZNF binding patterns and thus it is not clear if the binding code developed in vitro will be useful for identifying target genes of a particular ZNF. We performed genome-wide ChIP-seq for ZNF263, a C2H2 ZNF that contains 9 finger domains, a KRAB repression domain, and a SCAN domain and identified more than 5000 binding sites in K562 cells. Our results suggest that ZNF263 binds to a 24 nt site which differs from the motif predicted by the zinc finger code in several positions. Interestingly, many of the ZNF263 binding sites are located within the transcribed region of the target gene. Although ZNFs containing a KRAB domain are thought to function mainly as transcriptional repressors, many of the ZNF263 target genes are expressed at high levels. To address the biological role of ZNF263, we identified genes whose expression was altered by treatment of cells with ZNF263-specific siRNAs. Our results suggest that ZNF263 can have both positive and negative effects on transcriptional regulation of its target genes. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Examination of ZNF263 ChIP-seq in K562 cells.

2009-12-03 | E-GEOD-19235 | biostudies-arrayexpress

Genomic targets of the KRAB and scan domain-containing zinc finger protein 263 (ZNF263).

2009-11-24 | GSE19146 | GEO

Genomic targets of the KRAB and scan domain-containing zinc finger protein 263 (ZNF263).

2009-12-03 | GSE19235 | GEO

Whole exome sequencing of EGFR-TKI naive and EGFR-TKI resistant lung adenocarcinoma samples

Project description:Whole exome sequencing was performed on set of 48 DNA samples obtained from 16 EGFR mutated NSCLC patients whose tumors progressed following EGFR-TKI treatment. The DNA samples included baseline biopsy, rebiopsy and blood from the same patient. By comparing the variants in rebiopsy tumors and baseline tumors we aim to understand the genomic alterations responsible for the development of EGFR-TKI resistance in NSCLC patients.

2022-02-11 | E-MTAB-11404 | biostudies-arrayexpress

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