RNA-seq data (STAG2 WT and mutated Ewing sarcoma cell lines)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA721437 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:STAG2 is a member of cohesin complex and its gene is one of the most recurrently mutated in human cancer including in Ewing sarcoma. Here, we investigated STAG2 function in the context of Ewing sarcoma and performed transcriptome profiling of a panel of 15 WT and 15 mutated STAG2 established Ewing sarcoma cell lines.
2021-04-29 | GSE171948 | GEO
Project description:Ewing sarcoma is an aggressive malignancy characterized by oncogenic rearrangements of the EWS gene with an ETS-family transcription factor, most commonly FLI. Recent comprehensive next-generation sequencing efforts have revealed few other highly recurrent mutations in this disease apart from loss-of-function mutations in STAG2 which occur in 15-20% of tumors. STAG2 is a member of the cohesin complex, which regulates sister chromatid alignment during mitosis and epigenetic regulation of gene expression. While some studies suggest that loss of STAG2 is associated with the development of aneuploidy, this is not the case in Ewing sarcoma. To investigate whether STAG2 loss affects epigenetic regulation of gene expression in Ewing sarcoma, we developed isogenic Ewing sarcoma cell lines with STAG2 knockout. We found that Ewing sarcoma cells engineered for loss of STAG2 maintain an intact cohesion complex that alternately incorporates STAG1.
2021-05-14 | GSE165977 | GEO
Project description:Ewing sarcoma is an aggressive malignancy characterized by oncogenic rearrangements of the EWS gene with an ETS-family transcription factor, most commonly FLI. Recent comprehensive next-generation sequencing efforts have revealed few other highly recurrent mutations in this disease apart from loss-of-function mutations in STAG2 which occur in 15-20% of tumors. STAG2 is a member of the cohesin complex, which regulates sister chromatid alignment during mitosis and epigenetic regulation of gene expression. While some studies suggest that loss of STAG2 is associated with the development of aneuploidy, this is not the case in Ewing sarcoma. To investigate whether STAG2 loss effects epigenetic regulation of gene expression in Ewing sarcoma, we developed isogenic Ewing sarcoma cell lines with STAG2 knockout. We found that Ewing sarcoma cells engineered for loss of STAG2 maintain an intact cohesion complex that alternately incorporates STAG1.
2021-05-14 | GSE116494 | GEO
Project description:Ewing sarcoma is an aggressive malignancy characterized by oncogenic rearrangements of the EWS gene with an ETS-family transcription factor, most commonly FLI. Recent comprehensive next-generation sequencing efforts have revealed few other highly recurrent mutations in this disease apart from loss-of-function mutations in STAG2 which occur in 15-20% of tumors. STAG2 is a member of the cohesin complex, which regulates sister chromatid alignment during mitosis and epigenetic regulation of gene expression. While some studies suggest that loss of STAG2 is associated with the development of aneuploidy, this is not the case in Ewing sarcoma. To investigate whether STAG2 loss effects epigenetic regulation of gene expression in Ewing sarcoma, we developed isogenic Ewing sarcoma cell lines with STAG2 knockout. We found that Ewing sarcoma cells engineered for loss of STAG2 maintain an intact cohesion complex that alternately incorporates STAG1.
2021-05-14 | GSE116492 | GEO
Project description:Ewing sarcoma is an aggressive malignancy characterized by oncogenic rearrangements of the EWS gene with an ETS-family transcription factor, most commonly FLI. Recent comprehensive next-generation sequencing efforts have revealed few other highly recurrent mutations in this disease apart from loss-of-function mutations in STAG2 which occur in 15-20% of tumors. STAG2 is a member of the cohesin complex, which regulates sister chromatid alignment during mitosis and epigenetic regulation of gene expression. While some studies suggest that loss of STAG2 is associated with the development of aneuploidy, this is not the case in Ewing sarcoma. To investigate whether STAG2 loss effects epigenetic regulation of gene expression in Ewing sarcoma, we developed isogenic Ewing sarcoma cell lines with STAG2 knockout. We found that Ewing sarcoma cells engineered for loss of STAG2 maintain an intact cohesion complex that alternately incorporates STAG1.
2021-05-14 | GSE165783 | GEO
Project description:STAG2, a member of cohesin, is one of the most recurrently mutated genes in human cancer. Here, we investigated STAG2 function in the context of Ewing sarcoma, an aggressive bone tumor driven by EWS-FLI1 oncogene chimeric transcription factor. Five different Ewing sarcoma cell lines were transfected with siCT or 2 different siRNAs targeting STAG2 (siSA2#6 or siSA2#8). RNA in A673 & TC71 (siSTAG2) was extracted 24, 48 and 72 hours post-transfection. RNA in EW1, CHLA-10 and CHLA-258 (siSTAG2 and siEWSR1-FLI1) was extracted 72 hours post-transfection. RNA-seq based anlayses of these experiments highligted that STAG2 knock-down alters EWSR1-FLI1 activation signature.
2021-04-29 | GSE156653 | GEO
Project description:STAG2, a member of cohesin, is one of the most recurrently mutated genes in human cancer. Here, we investigated STAG2 function in the context of Ewing sarcoma, an aggressive bone tumor driven by EWS-FLI1 oncogene chimeric transcription factor. A673 Ewing sarcoma cell line was trasfected with siCT or 2 different siRNA targetting STAG2 during 72h and CTCF HiChIP experiments were preformed for each conditions. Analyses of HiChIP data show that STAG2 knowck-down alters CTCF-anchored loop extrusion.
2021-04-29 | GSE156650 | GEO
Project description:STAG2, a member of cohesin, is one of the most recurrently mutated genes in human cancer. Here, we investigated STAG2 function in the context of Ewing sarcoma. Using a CRISPR/Cas9 approach, we generated two STAG2 knock-out isogenic clones (A673_SA2m#1 and TC71_SA2m#2) derived from A673 and TC71 STAG2 wild type (WT) Ewing sarcoma cell line. A STAG2 rescue model (A673_SA2r) was generated by correcting the CRISPR mutation in the A673_SA2m#1 model. These STAG1/2 proficient and deficient models were profiled by CTCF HiChIP experiments. STAG2 isogenic models were also profiled by H3K27ac HiChIP experiments. Analyses of HiChIP data allowed to show that STAG2 promotes CTCF-anchored loop extrusion and cis-promoter and -enhancer interactions.
2021-04-29 | GSE133227 | GEO
Project description:SMC1a HiChIP was performed for the Ewing sarcoma cell line A673 under two conditions: 1) cells treated with non-targeting CRISPR Cas9 guides or 2) STAG2-targeting CRISPR Cas9 guides. Cells treated for gene editing were clonally selected and confirmed to either express STAG2 (control condition) or have loss of STAG2 expression (STAG2 loss condition). For the control condition, we used the cell clones A673.sgNT-1c4 and the STAG2 knockout clone A673.sgSTAG2-1c6. HiChIP was performed for each clone in duplicate.
2021-05-14 | GSE113100 | GEO
Project description:STAG2, a member of cohesin, is one of the most recurrently mutated genes in human cancer. Here, we investigated STAG2 function in the context of Ewing sarcoma, an aggressive bone tumor driven by EWS-FLI1 oncogene chimeric transcription factor. Using a CRISPR/Cas9 approach, we generated three STAG2 knock-out isogenic clones (A673_SA2m#1, TC71_SA2m#1 and TC71_SA2m#2) derived from A673 and TC71 STAG2 wild type (WT) Ewing sarcoma cell line. Similarly, a STAG1 knock-out isogenic clone (A673_SA1m#1) was generated. Finally, a STAG2 rescue model (A673_SA2r) was generated by correcting the CRISPR mutation in the A673_SA2m#1 model. These STAG1/2 proficient and deficient models were profiled by ChIP-seq for EWS-FLI1, CTCF, cohesin members, and histone marks and allowed to highlight a global conservation of binding for these marks upon STAG2 mutation.
2021-04-29 | GSE133154 | GEO