The transcriptional profile of A673 parental and SP-2509 Drug resistant cells treated with DMSO and SP-2509 (2uM 48hrs) Overall design: A673 parental and SP-2509 Drug resistant cells treated with DMSO and SP-2509 (2uM 48hrs)
Ewing sarcoma resistance to SP-2509 is not mediated through KDM1A/LSD1 mutation.
Treatment, Subject
View SamplesThe transcriptional profile of A673 parental, and SP-2509 drug resistant washout cells (4 and 6 months) Overall design: Following generation of A673 SP-2509 drug resistant cells (chronic exposure for 7 months), drug was withdrawn with cell pellets collected 4 and 6 months after removal.
Ewing sarcoma resistance to SP-2509 is not mediated through KDM1A/LSD1 mutation.
Disease, Treatment, Subject
View SamplesThe human SYT-SSX fusion protein was expressed in a developmentally dependent fashion in murine myoblasts. Tumors harvested from mice in adolescence were compared to normal mouse skeletal muscle samples.
A conditional mouse model of synovial sarcoma: insights into a myogenic origin.
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View SamplesThis SuperSeries is composed of the SubSeries listed below.
Expression profiling of EWS/FLI identifies NKX2.2 as a critical target gene in Ewing's sarcoma.
No sample metadata fields
View SamplesA673 Ewing's sarcoma cells, with inducible EWS/FLI cDNA, harboring the EF-2-RNAi retrovirus, induced (or uninduced) for the indicated time period.
Expression profiling of EWS/FLI identifies NKX2.2 as a critical target gene in Ewing's sarcoma.
No sample metadata fields
View SamplesA673 Ewing's sarcoma cells containing either control RNAi retroviral constructs (luc-RNAi), or RNAi retroviral constructs targeting the endogenous EWS/FLI fusion transcript (either EF-2-RNAi or EF-4-RNAi).
Expression profiling of EWS/FLI identifies NKX2.2 as a critical target gene in Ewing's sarcoma.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Sparstolonin B inhibits pro-angiogenic functions and blocks cell cycle progression in endothelial cells.
Specimen part, Treatment
View SamplesSparstolonin B is a novel bioactive compound isolated from Sparganium stoloniferum, an herb historically used in Traditional Chinese Medicine as an anti-tumor agent. SsnB has previously demonstrated anti-angiogenic properties. In functional assays, SsnB inhibited endothelial cell tube formation (Matrigel method) and cell migration (Transwell method) in a dose-dependent manner.
Sparstolonin B inhibits pro-angiogenic functions and blocks cell cycle progression in endothelial cells.
Specimen part, Treatment
View SamplesSparstolonin B is a novel bioactive compound isolated from Sparganium stoloniferum, an herb historically used in Traditional Chinese Medicine as an anti-tumor agent. SsnB has previously demonstrated anti-angiogenic properties. In functional assays, SsnB inhibited endothelial cell tube formation (Matrigel method) and cell migration (Transwell method) in a dose-dependent manner.
Sparstolonin B inhibits pro-angiogenic functions and blocks cell cycle progression in endothelial cells.
Specimen part, Treatment
View SamplesThe purpose of this study was to define biomarkers of sensitivty and mechanisms of resistance to the KDM1A/LSD1 inhibtor SP-2509 (HCI-2509) in Ewing sarcoma cell lines. We report that regardless of drug sensitivity all cell lines engage the UPR and ER-stress response following treatment with SP-2509 resulting in apoptotic cytotoxicity. In addition hypersentsitive cell lines shared a common basal transcriptnomic profile, with hypersensitive cell lines signficantly inducing ETS1 which was not observed in sensitive cell lines. Overall design: 6 Ewing sarcoma cell lines were treated with either vehicle control (DMSO) or the reversible LSD1/KDM1A inhibitor SP-2509 (2uM) for 48hrs. Three SP-2509 hypersensitive (IC50< 300nM)(A673, TC32, TC252) and three SP-2509 sensitive (IC50>900nM) (EWS-502, ES-2 and TC71) cell lines were investigated. Paired RNA from three indpendent experiments per cell line was analyzed.
Therapeutic Targeting of KDM1A/LSD1 in Ewing Sarcoma with SP-2509 Engages the Endoplasmic Reticulum Stress Response.
Treatment, Subject
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