Expression profiling in STAG2 mutant K562 cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA543745 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9090320_1.fastq.gz | Fastqsanger.gz | |||
| SRR9090320_2.fastq.gz | Fastqsanger.gz | |||
| SRR9090311_1.fastq.gz | Fastqsanger.gz | |||
| SRR9090311_2.fastq.gz | Fastqsanger.gz | |||
| SRR9090321_1.fastq.gz | Fastqsanger.gz |
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Project description:Chromatin accessibility profiling in STAG2 mutant K562 cells
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Project description:K562 (female chronic myelogenous leukemia) cells were CRISPR-Cas9 edited to contain STAG2 R614* mutation. STAG2 is encoded on the X-chromosome and normally mutation on one allele is sufficient for complete loss of STAG2 protein due to the wild type allele being mosaically silenced. However, we obtained both heterozygous and homozygous mutant lines that showed partial and complete loss of STAG2 protein respectively. We here examined the impact of STAG2 R614* mutation on gene expression and chromatin acessibilty.
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Project description:Chromatin accessibility and expression profiling in STAG2 mutant K562 cells
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Project description:K562 (female chronic myelogenous leukemia) cells were CRISPR-Cas9 edited to contain STAG2 R614* mutation. STAG2 is encoded on the X-chromosome and normally mutation on one allele is sufficient for complete loss of STAG2 protein due to the wild type allele being mosaically silenced. However, we obtained both heterozygous and homozygous mutant lines that showed partial and complete loss of STAG2 protein respectively. We here examined the impact of STAG2 R614* mutation on gene expression and chromatin acessibilty.
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Project description:MCF10A cells were CRISPR-Cas9 edited to create heterozygous deletion in RAD21 and SMC3 subunits of cohesin. STAG2 is on the X chromosome, hence CRISPR-Cas9 editing resulted in complete loss of STAG2. Total RNA was sequenced from the MCF10A parental and cohesin mutant MCF10A lines. The acute megakaryoblastic leukaemia cell line CMK was CRISPR-Cas9 edited to cotain STAG2 R614* mutation. CRISPR-Cas9 edited STAG2 mutant line showed complete loss of STAG2. CMK parental and the STAG2 mutant line were treated with Wnt3a for 4 hours and total RNA was sequenced at in the control or non-treated (con) and following 4 hours of Wnt3a treatment (Wnt3a4hr).
2020-12-13 | GSE154086 | GEO
Project description:We performed ATAC-sequencing in LSK cells (Lin(neg)/c-Kit(+)/Sca-1(+)) from shRNA mice carrying an shRNA for either Renilla or Stag2. ATAC-sequencing control (Renilla) and Stag2 knockdown cells.
2015-09-16 | E-GEOD-72367 | biostudies-arrayexpress
Project description:We have discovered frequent genetic inactivation of the STAG2 gene in diverse human cancers including glioblastoma, Ewing's sarcoma, and melanoma. STAG2 encodes a subunit of the sister chromatid cohesion complex called the "cohesin complex" that is responsible for the cohesion of sister chromatids following DNA replication and is cleaved at the metaphase to anaphase transition to enable chromosome segregation into daughter cells. Interestingly, the cohesin complex has also been implicated as a regulator of chromatin architecture and transcription. To determine the functional significance of STAG2 inactivation in cancer pathogenesis, we used somatic cell gene targeting to correct the endogenous mutations of STAG2 in two aneuploid human glioblastoma cell lines, H4 and 42MGBA. Similarly, somatic cell gene targeting was also used to introduce a nonsense mutation into codon 6 of the endogenous wild-type allele of STAG2 in HCT116 cells, a near-diploid human colorectal cancer cell line with stable karyotype. Expression profiling of these three paired sets of STAG2-proficient and deficient cells demonstrated that STAG2 does not play a global role in transcriptional regulation nor does it recurrently modulate the expression of specific tumor-promoting or suppressing genes. For further details, see Solomon et al., Mutational inactivation of STAG2 causes aneuploidy in human cancer.
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Project description:Transcriptome profiling of NGLY1 deficient K562 cells
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Project description:Inactivating mutations of genes encoding the cohesin complex are common in a wide range of human cancers. STAG2 is the most commonly mutated subunit. Here we report the impact of stable correction of endogenous, naturally occurring STAG2 mutations on gene expression, 3D genome organization, chromatin loops, and Polycomb signaling in glioblastoma multiforme. Correction of mutant STAG2 significantly altered the expression of ~10% of all expressed genes. The genes most highly regulated by STAG2 (e.g. FGF7, c-KIT, MAGE tumor antigens) were virtually all upregulated in STAG2-mutant cells. Hi-C revealed that ~3% of A/B compartments switched after STAG2 correction, and confirmed prior findings that STAG2 is dispensable for maintenance of Topologically Associating Domains (TADs). The size and strength of thousands of chromatin loops were altered by STAG2 correction, a subset of which controlled the expression of adjacent genes. Loops specific to STAG2-mutant cells and tumors were very large, supporting prior findings that STAG1-containing cohesin complexes have greater loop extrusion processivity than STAG2-containing cohesin complexes, and suggesting that long loops may be a generalizable feature of STAG2-mutant cancers. Finally, STAG2-regulated chromatin loops were enriched for the H3K27me3 Polycomb epigenetic mark, revealing that inactivation of STAG2 can activate Polycomb signaling in GBM. Together these findings illuminate the landscape of STAG2-regulated genes, A/B compartments, chromatin loops, and pathways in GBM, providing important clues into the still mysterious mechanism of STAG2 tumor suppression in human cancer.
2024-05-07 | GSE240343 | GEO
Project description:STAG2 is targeted by somatic aberrations in a subset (4%) of human PDAs. Transposon mediated disruption of STAG2 in a KRASG12D genetically engineered mouse model promotes the development of PDA and its progression to metastatic disease. There was a statistically significant loss of STAG2 protein expression in human tumor tissue (Wilcoxon-Rank test) with complete absence of STAG2 staining observed in 15 (4.3%) patients. In univariate Kaplan Meier analysis nearly complete STAG2 positive staining (> 95% of nuclei positive) was associated with a median survival benefit of 6.41 months (p = 0.031). The survival benefit of adjuvant chemotherapy was only seen in patients with a STAG2 staining of less than 95% (median survival benefit 7.65 months; p = 0.028). Multivariate Cox Regression analysis showed that STAG2 is an independent prognostic factor for survival in pancreatic cancer patients. Finally we show that RNAi mediated knockdown of STAG2 selectively sensitizes human PDA cell lines to platinum-based therapy. We used DNA content flow sorting to identify and purify tumor nuclei of PDA samples from 50 patients. The genome of each sorted sample was profiled by oligonucleotide comparative genomic hybridization (aCGH) and targeted resequencing of STAG2. Transposon insertions within STAG2 in a KRASG12D driven genetically engineered mouse (GEM) model of PDA were screened by RT-PCR. We then used a tissue microarray (TMA) to survey STAG2 protein expression levels in 344 human PDA tumor samples and adjacent tissues. Univariate Kaplan Meier analysis and multivariate Cox Regression analysis was used to assess the association of STAG2 expression relative to overall survival and responses to adjuvant therapy. Finally RNAi based assays with PDA cell lines were used to assess the potential therapeutic consequence of STAG2 expression in responses to 18 therapeutic agents.
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