Transcription factor ZBTB7A-deficiency effect on U87MG cells in vitro
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA804312 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17930451_1.fastq.gz | Fastqsanger.gz | |||
| SRR17930451_2.fastq.gz | Fastqsanger.gz | |||
| SRR17930452_1.fastq.gz | Fastqsanger.gz | |||
| SRR17930452_2.fastq.gz | Fastqsanger.gz | |||
| SRR17930453_1.fastq.gz | Fastqsanger.gz |
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Project description:Analysis of glioblastoma cell line U87MG depleted for ZBTB7A (Zinc Finger and BTB Domain Containing 7A, also known as FBI1, POKEMON or LRF). ZBTB7A is transcription factor that represses the transcription of a wide range of genes involved in cell proliferation and differentiation. Results provide insight into the role of ZBTB7A in glioblastoma.
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Project description:Differential transcriptome analysis between control cells (U87MG), TMZ-resistant cells with continuous TMZ treatment (U87MG R50) and TMZ-resistant cells with interrupted treatment (U87MG OFF R50).
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Project description:Zinc finger and BTB domain containing transcription repressor ZBTB7A has been recently reported as a tumor suppressor who plays important functions to prevent the progression of prostate cancer. However, the chromatin activity of ZBTB7A in prostate cancer cells remain unclear. In order to identify the cistrome and transcriptome of ZBTB7A, we performed ZBTB7A ChIP-seq in VCaP cells and RNA-seq in VCaP cells transfected with siRNA targeting ZBTB7A or non-targeting control, respectively (cells were grown in full serum). By using combined ChIP-seq and RNA-seq analyses in VCaP cells, we have precisely mapped the ZBTB7A binding sites and identified a subset of genes that are directly repressed by ZBTB7A. To study the chromatin interaction of ZBTB7A with androgen receptor (AR), we also performed ChIP-seq of ZBTB7A in VCaP cells stimulated with 10 nM DHT for 4 hours versus vehicle control (cells were hormone-depleted prior to DHT stimulation). Our results show that ZBTB7A binding is increased by androgen at AR and ZBTB7A overlapping sites.
2019-09-12 | GSE123089 | GEO
Project description:Zinc finger and BTB domain containing transcription repressor ZBTB7A has been recently reported as a tumor suppressor who plays important functions to prevent the progression of prostate cancer. However, the chromatin activity of ZBTB7A in prostate cancer cells remain unclear. In order to identify the cistrome and transcriptome of ZBTB7A, we performed ZBTB7A ChIP-seq in VCaP cells and RNA-seq in VCaP cells transfected with siRNA targeting ZBTB7A or non-targeting control, respectively (cells were grown in full serum). By using combined ChIP-seq and RNA-seq analyses in VCaP cells, we have precisely mapped the ZBTB7A binding sites and identified a subset of genes that are directly repressed by ZBTB7A. To study the chromatin interaction of ZBTB7A with androgen receptor (AR), we also performed ChIP-seq of ZBTB7A in VCaP cells stimulated with 10 nM DHT for 4 hours versus vehicle control (cells were hormone-depleted prior to DHT stimulation). Our results show that ZBTB7A binding is increased by androgen at AR and ZBTB7A overlapping sites.
2019-09-12 | GSE123090 | GEO
Project description:Tumor budding (TB), clusters of less than 5 cells dissociated from the tumor mass, is reported to predict nodal involvement and recurrence in multiple human cancers including gastric carcinoma (GC). However, it is not clear how TB forms. In this study, we determined the expression pattern of GAGE12I, CTNND1, Kif26B, CREB1 and ZBTB7A in human GC samples by IHC attempting to find any TB-related markers. The results showed that TB could predict lymph node metastasis and is negatively associated with the overall survival of GC patients. The expression of ZBTB7A in the tumor margin (invasive front), rather than the other four markers, was much higher than that inside the tumor and was positively correlated with TB score. Moreover, patients with higher marginal ZBTB7A expression had poorer prognosis. ZBTB7A could enhance the migration and invasion capabilities of GC cells in vitro. Mechanically, ZBTB7A might activate EGFR-MAPK-ERK and PI3K-AKT-mTOR pathway, which resulted in epithelial-mesenchymal transition (EMT) to induce the formation of TB. Thus, we concluded that higher ZBTB7A expression in the tumor margin may contribute to the dissociation of tumor cells from the tumor mass to form TB by initiating EMT via EGFR-MEK-ERK and PI3K-AKT-mTOR pathway.
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Project description:U87MG is a glioblastoma cell line that shows substantial heterogeneity despite long-term passaging. We used microarrays to identify variations in gene expression that are associated with phenotypic differences among subclones derived from U87MG.
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Project description:Hemoglobinopathies, including sickle cell disease and _-thalassemia, are global public health concerns. Induction of fetal-type hemoglobin (HbF) is a promising means to treat these disorders; however, precisely how HbF expression is silenced in adult erythroid cells is not fully understood. Here, we show that the LRF/ZBTB7A transcription factor is a potent repressor of HbF production. LRF inactivation derepresses embryonic/fetal _-globin expression in mouse and human adult erythroid cells. We employed genome-wide analysis of the transcriptome, chromatin accessibility and LRF occupancy sites, and demonstrate that LRF occupies the _-globin loci and maintains nucleosome density necessary for _-globin silencing. LRF confers its repressive activity through a unique NuRD repressor complex independent of BCL11A. Strikingly, human erythroid lines lacking both LRF and BCL11A exhibited almost a complete switch in expression from adult- to fetal-type globin, suggesting that these two factors cumulatively represent the near entirety of _-globin repressive activity in adult erythroid cells. RNA-seq, LRF ChIP-seq and ATAC-seq assays were used to investigtae LRF binding, effect of LRF depletion on transcription and chromatin landscape in mouse and human cells.
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Project description:We previously identified KDM5B, encoding a histone H3 lysine 4 (H3K4) demethylase, as an oncogene in estrogen receptor positive (ER+) breast cancer driving endocrine resistance. Here we describe that KDM5A is frequently amplified and overexpressed in basal breast tumors and is associated with chemotherapy resistance. Using CRISPR knockout viability screens -/+ KDM5 inhibition (KDM5i), we found that deletion of the transcription factor ZBTB7A and core SAGA complex increased sensitivity to KDM5i, whereas knockout of RHO-GTPases led to resistance. Integrated ChIP-seq and RNA-seq analyses revealed colocalization of ZBTB7A and KDM5s at promoters with high H3K4me3 signal and dependence of KDM5A binding on ZBTB7A. ZBTB7A knockout had a pleiotropic effect on transcriptional responses to KDM5i, in which it modulates the KDM5i-induced innate immune signaling and NF-kB-regulated genes. ZBTB7A knockout and KDM5i cooperate to alter cell states with KDM5i decreasing basal-like and ZBTB7A knockout inducing mesenchymal-like gene expression patterns. Our work furthers our understanding of KDM5-mediated gene regulation in breast cancer and identifies key pathways that mediate sensitivity to KDM5 inhibition
2024-10-14 | GSE259249 | GEO
Project description:We previously identified KDM5B, encoding a histone H3 lysine 4 (H3K4) demethylase, as an oncogene in estrogen receptor positive (ER+) breast cancer driving endocrine resistance. Here we describe that KDM5A is frequently amplified and overexpressed in basal breast tumors and is associated with chemotherapy resistance. Using CRISPR knockout viability screens -/+ KDM5 inhibition (KDM5i), we found that deletion of the transcription factor ZBTB7A and core SAGA complex increased sensitivity to KDM5i, whereas knockout of RHO-GTPases led to resistance. Integrated ChIP-seq and RNA-seq analyses revealed colocalization of ZBTB7A and KDM5s at promoters with high H3K4me3 signal and dependence of KDM5A binding on ZBTB7A. ZBTB7A knockout had a pleiotropic effect on transcriptional responses to KDM5i, in which it modulates the KDM5i-induced innate immune signaling and NF-kB-regulated genes. ZBTB7A knockout and KDM5i cooperate to alter cell states with KDM5i decreasing basal-like and ZBTB7A knockout inducing mesenchymal-like gene expression patterns. Our work furthers our understanding of KDM5-mediated gene regulation in breast cancer and identifies key pathways that mediate sensitivity to KDM5 inhibition
2024-10-14 | GSE259248 | GEO
Project description:EGFRvA is a novel and widely-expressed EGFR isoform, whose upregulation is positively related to glioma grades. Intriguingly, it is the upregulation of EGFRvA but not EGFR that significantly correlates with a poor prognosis in glioma patients. Cancer cells expressing EGFRvA (relative to EGFR) display a higher invasive capacity and a lower sensitivity to EGFR tyrosine kinase inhibitors (TKIs). To investigate the significant differently expressed genes between U87MG EGFRvA cells and U87MG EGFR cells，microarray experiments were conducted.
2012-09-30 | GSE41230 | GEO