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Transcription factor ZIC2 regulates tumorigenic phenotypes in epithelial ovarian cancer in a context-dependent manner

ABSTRACT: Transcription factor ZIC2 regulates tumorigenic phenotypes in epithelial ovarian cancer in a context-dependent manner

PROVIDER: PRJNA944966 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23869348_1.fastq.gz	Fastqsanger.gz
	SRR23869348_2.fastq.gz	Fastqsanger.gz
	SRR23869349_1.fastq.gz	Fastqsanger.gz
	SRR23869349_2.fastq.gz	Fastqsanger.gz
	SRR23869350_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Transcription factor ZIC2 regulates tumorigenic phenotypes in epithelial ovarian cancer in a context-dependent manner

Project description:Transcription factor ZIC2 plays a pro-tumorigenic role in several human cancers. Herein, we demonstrate that elevated ZIC2 expression was associated with lower overall and post-progression survival of epithelial ovarian cancer (EOC) patients. Knockout of ZIC2 in EOC cells attenuated tumorigenic phenotypes in vitro and in vivo, indicating a pro-tumorigenic role for ZIC2 in EOC. On the other hand, however, overexpression of ZIC2 in EOC cells that do not express endogenous ZIC2 promoted cell migration and sphere formation, but inhibited cell growth and colony formation in vitro and tumor growth in vivo, indicating a context-dependent function for ZIC2 in EOC. Transcriptomic study showed that ZIC2-regulated genes were involved in multiple biological processes and signaling pathways associated with tumor progression and that ZIC2 regulated common or distinct genes in ZIC2 knockout and overexpression models, which explains the consistency and discrepancy in ZIC2 functions observed in the two models. In conclusion, our findings reveal a context-dependent role for ZIC2 in regulating tumorigenic phenotypes in EOC, providing evidence that ZIC2 can be a potential therapeutic target for EOCs that express a high level of ZIC2.

2024-05-01 | GSE227395 | GEO

Mutant p53 elicits context-dependent pro-tumorigenic phenotypes

Project description:Mutant p53 elicits context-dependent pro-tumorigenic phenotypes

| PRJNA660971 | ENA

Mutant p53 elicits context-dependent pro-tumorigenic phenotypes (microarray)

Project description:Mutant p53 elicits context-dependent pro-tumorigenic phenotypes (microarray)

| PRJNA660982 | ENA

Mutant p53 elicits context-dependent pro-tumorigenic phenotypes (ChIP-Seq)

Project description:Mutant p53 elicits context-dependent pro-tumorigenic phenotypes (ChIP-Seq)

| PRJNA660969 | ENA

Zic2, an enhancer-binding factor required for embryonic stem cell specification

Project description:The Zinc finger protein of the cerebellum 2 (Zic2) is one of the vertebrate homologs of the Drosophila pair-rule gene odd-paired (opa). Our molecular and biochemical studies have demonstrated that Zic2 to preferentially bind to transcriptional enhancers and functions as a cofactor that interacts with the NuRD complex in ES cells. Detailed genome-wide studies demonstrate that Zic2 function with Mbd3/NuRD in regulating the chromatin state and transcriptional output of genes linked to differentiation. Zic2 is dispensable for the selfrenewal of ES cells but is required for proper differentiation, similar to what has been previously reported for Mbd3/NuRD. Our study identifies Zic2 as a key factor in the execution of the pluripotency program with Mbd3/NuRD in ES cells. ChIP-seq of Zic2, Chd4, Mbd3 and Zic3 in mES cells. ChIP-seq of H3K27me3, H3K27ac, H3K4me3, H3K4me1 and PolII in mES cells after Zic2 shRNA and non-targeting shRNA. RNA-seq of mES cells after Zic2, Zic3, Mbd3 and Mta2 shRNA and non-targeting shRNA.

2015-02-23 | E-GEOD-61188 | biostudies-arrayexpress

Identification of ZIC2 target genes in human pancreatic cancer cell lines PANC-1 and KP-4

Project description:PANC-1Tet/ZIC2 and PANC-1Tet/empty were established from human pancreatic cancer cell line PANC-1. PANC-1Tet/ZIC2 cells express FLAG-tagged human ZIC2 on the withdrawal of DOX. On the other hand, PANC-1Tet/empty was transfected an empty vector for the control experiment. To identify ZIC2 target genes, total RNAs were purified from the cells before and 48 hours after the DOX withdrawal. Gene expression profiles were analyzed by AGILENT human 4x44k cDNA microarray. As well as ZIC2-inducible system, we performed ZIC2-knockdown experiments in PANC-1 human pancreatic cancer cells. After 96 hours transfection of siRNAs for ZIC2 and its control, total RNAs were purified and gene expression profiles were analyzed by AGILENT human 4x44k cDNA microarray. ZIC2 target genes were identified in PANC-1 cells. Gene expression profiles of PANC-1Tet/ZIC2 and PANC-1Tet/empty cells were analyzed by AGILENT human 4x44k cDNA microarray before and 48 hours after the DOX withdrawal. As well as ZIC2-inducible system, gene expression profiles of control- and ZIC2-knocdown PANC-1 cells were also analyzed by AGILENT human 4x44k cDNA microarray.

2014-04-14 | E-GEOD-39704 | biostudies-arrayexpress

ZIC2 ChIP-Seq in KSHV latent and lytic reactivated BCBL-1 cells

Project description:ZIC2 is required for the maintenance of KSHV latency in human host cells. To understand the molecular action of ZIC2, we map ZIC2 binding sites across the KSHV genome in BCBL-1 cells using ChIP-Seq analysis.

2017-08-25 | GSE102462 | GEO

ARID1A-BAF coordinates ZIC2 genomic occupancy for epithelial to mesenchymal transition in cranial neural crest lineage commitment.

Project description:The BAF chromatin remodeler regulates lineage commitment including cranial neural crest cell (CNCC) specification. BAF subunit mutations cause Coffin-Siris Syndrome (CSS), a congenital disorder characterized by distinct craniofacial features and intellectual disability. Approximately 50% of CSS patients carry mutations in one of the mutually exclusive BAF subunits, ARID1A/ARID1B. While Arid1a deletion in mouse neural crest causes severe craniofacial phenotypes, little is known about the role of ARID1A in CNCC specification. Using CSS patient-derived ARID1A+/- iPSCs to model CNCC specification, we discovered that ARID1A-haploinsufficency impairs epithelial to mesenchymal transition (EMT), a process necessary for CNCC delamination and migration from the neural tube. Furthermore, wild-type ARID1A-BAF regulates enhancers associated with EMT genes. ARID1A-BAF binding at these enhancers is impaired in heterozygotes, while binding at promoters is unaffected. At the sequence level, these EMT enhancers contain binding motifs for ZIC2, and ZIC2 binding at these sites is ARID1A-dependent. When excluded from EMT enhancers, ZIC2 relocates to neuronal enhancers, triggering aberrant neuronal gene activation. In mice, deletion of Zic2 impairs NCC delamination, while ZIC2 overexpression in chick embryos at pre-migratory neural crest stages elicits abnormal cell delamination from the neural tube. These findings reveal a novel ARID1A-ZIC2 axis essential for EMT and CNCC delamination.

2024-07-23 | GSE261846 | GEO

Zic2, an enhancer-binding factor required for embryonic stem cell specification

2015-02-23 | GSE61188 | GEO

Mutant p53 elicits context-dependent pro-tumorigenic phenotypes.

Project description:The tumor suppressor gene TP53 is the most frequently mutated gene in numerous cancer types, including prostate cancer (PCa). Specifically, missense mutations in TP53 are selectively enriched in PCa, and cluster to particular "hot spots" in the p53 DNA binding domain with mutation at the R273 residue occurring most frequently. While this residue is similarly mutated to R273C-p53 or R273H-p53 in all cancer types examined, in PCa selective enrichment of R273C-p53 is observed. Importantly, examination of clinical datasets indicated that TP53 heterozygosity can either be maintained or loss of heterozygosity (LOH) occurs. Thus, to mimic tumor-associated mutant p53, R273C-p53 and R273H-p53 isogenic PCa models were developed in the presence or absence of wild-type p53. In the absence of wild-type p53, both R273C-p53 and R273H-p53 exhibited similar loss of DNA binding, transcriptional profiles, and loss of canonical tumor suppressor functions associated with wild-type p53. In the presence of wild-type p53 expression, both R273C-p53 and R273H-p53 supported canonical p53 target gene expression yet elicited distinct cistromic and transcriptional profiles when compared to each other. Moreover, heterozygous modeling of R273C-p53 or R273H-p53 expression resulted in distinct phenotypic outcomes in vitro and in vivo. Thus, mutant p53 acts in a context-dependent manner to elicit pro-tumorigenic transcriptional profiles, providing critical insight into mutant p53-mediated prostate cancer progression.

| S-EPMC8755525 | biostudies-literature

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