Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-6461
PROVIDER: PRJNA98691 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Synovial sarcoma is a rare malignancy characterized by the presence of a specific chromosomal translocation t(X;18) that results in the formation of a fusion protein SYT-SSX. Because it is believed that synovial sarcoma arises from mesenchymal stem or progenitor cells, we wanted to determine the changes in gene expression caused by SYT-SSX2 in untransformed mesenchymal progenitor cells - murine C2C12 myoblasts in this experiment.
2011-09-26 | GSE26562 | GEO
Project description:Synovial sarcoma is a rare malignancy characterized by the presence of a specific chromosomal translocation t(X;18) that results in the formation of a fusion protein SYT-SSX. Because it is believed that synovial sarcoma arises from mesenchymal stem or progenitor cells, we wanted to determine the changes in gene expression caused by SYT-SSX2 in untransformed mesenchymal progenitor cells - murine C2C12 myoblasts in this experiment. In 2 independent experiments, C2C12 myoblasts were infected with retrovirus carrying either control vector (pOZ) or SYT-SSX2 expression vector. Total cellular RNA was extracted 48 hours post-infection and utilized for microarray analysis on Affymetrix arrays.
2011-09-25 | E-GEOD-26562 | biostudies-arrayexpress
Project description:Cellular identity is determined by its gene expression programs. The ability of the cell to change its identity and produce cell types outside its lineage is achieved by the activity of transcription controllers capable of reprogramming differentiation gene networks. The synovial sarcoma associated protein, SYT-SSX2, reprograms myogenic progenitors and human bone marrow-derived mesenchymal stem cells (BMMSCs) by dictating their commitment to a pro-neural lineage. It fulfills this function by directly targeting an extensive array of neural-specific genes as well as genes of developmental pathway mediators. Concomitantly, the ability of both myoblasts and BMMSCs to differentiate into their normal myogenic and adipogenic lineages was compromised. Synovial sarcoma is believed to arise in mesenchymal stem cells where formation of the t(X;18) translocation product, SYT-SSX, constitutes the primary event in the cancer. SYT-SSX is therefore believed to initiate tumorigenesis in its target stem cell. The data presented here allow a glimpse at the initial events that likely occur when SYT-SSX2 is first expressed and its dominant function in subverting the nuclear program of the stem cell, leading to its aberrant differentiation, as a first step toward transformation. In addition, we identified the fibroblast growth factor receptor gene, Fgfr2, as one occupied and upregulated by SYT-SSX2. Knockdown of FGFR2 in both BMMSCs and synovial sarcoma cells abrogated their growth and attenuated their neural phenotype. These results support the notion that the SYT-SSX2 nuclear function and differentiation effects are conserved throughout sarcoma development and are required for its maintenance beyond the initial phase. They also provide the stem cell regulator, FGFR2 as a promising candidate target for future synovial sarcoma therapy. Refer to individual Series
2011-09-25 | E-GEOD-26565 | biostudies-arrayexpress
Project description:Synovial sarcoma is a rare malignancy characterized by the presence of a specific chromosomal translocation t(X;18) that results in the formation of a fusion protein SYT-SSX. Because it is believed that synovial sarcoma arises from mesenchymal stem or progenitor cells, we used human bone marrow-derived mesenchymal stem cells (MSCs) to determine the changes in gene expression caused by this oncogene in untransformed MSCs.
2011-09-26 | GSE26563 | GEO
Project description:Synovial sarcoma is a rare malignancy characterized by the presence of a specific chromosomal translocation t(X;18) that results in the formation of a fusion protein SYT-SSX. Because it is believed that synovial sarcoma arises from mesenchymal stem or progenitor cells, we used human bone marrow-derived mesenchymal stem cells (MSCs) to determine the changes in gene expression caused by this oncogene in untransformed MSCs. In 2 independent experiments, human bone marrow-derived MSCs were infected with retrovirus carrying either control vector (pOZ) or SYT-SSX2 expression vector. Total cellular RNA was extracted 4 days post-infection and utilized for microarray analysis on Affymetrix arrays.
2011-09-25 | E-GEOD-26563 | biostudies-arrayexpress
Project description:Cellular identity is determined by its gene expression programs. The ability of the cell to change its identity and produce cell types outside its lineage is achieved by the activity of transcription controllers capable of reprogramming differentiation gene networks. The synovial sarcoma associated protein, SYT-SSX2, reprograms myogenic progenitors and human bone marrow-derived mesenchymal stem cells (BMMSCs) by dictating their commitment to a pro-neural lineage. It fulfills this function by directly targeting an extensive array of neural-specific genes as well as genes of developmental pathway mediators. Concomitantly, the ability of both myoblasts and BMMSCs to differentiate into their normal myogenic and adipogenic lineages was compromised. Synovial sarcoma is believed to arise in mesenchymal stem cells where formation of the t(X;18) translocation product, SYT-SSX, constitutes the primary event in the cancer. SYT-SSX is therefore believed to initiate tumorigenesis in its target stem cell. The data presented here allow a glimpse at the initial events that likely occur when SYT-SSX2 is first expressed and its dominant function in subverting the nuclear program of the stem cell, leading to its aberrant differentiation, as a first step toward transformation. In addition, we identified the fibroblast growth factor receptor gene, Fgfr2, as one occupied and upregulated by SYT-SSX2. Knockdown of FGFR2 in both BMMSCs and synovial sarcoma cells abrogated their growth and attenuated their neural phenotype. These results support the notion that the SYT-SSX2 nuclear function and differentiation effects are conserved throughout sarcoma development and are required for its maintenance beyond the initial phase. They also provide the stem cell regulator, FGFR2 as a promising candidate target for future synovial sarcoma therapy. This SuperSeries is composed of the SubSeries listed below.
2011-09-26 | GSE26565 | GEO
Project description:Synovial sarcoma is a rare malignancy that is characterized by the presence of a chromosomal translocation t(X;18). This genetic abnormality results in the fusion of 2 transcriptional co-regulators, SYT and SSX, which have been shown to mediate transcriptional activation and repression, respectively. Although the fusion protein does not bind DNA directly, SYT-SSX2 is known to function through interaction with chromatin-modifying complexes. In this study, we wanted to determine the SYT-SSX2 occupancy across the whole genome in order to further characterize its function by identifying genes that may be deregulated by this protein. C2C12 myoblasts were infected with retrovirus carrying SYT-SSX2-HA-FLAG expression vector. Chromatin immunoprecipitation (ChIP) was performed on cell lysates with either control IgG antibody (Abcam) or anti-FLAG antibody (Sigma). Lysates from 2 independent infections were pooled and used to isolate control ChIP DNA (IgG). DNA from 2 independent FLAG ChIP experiments (each using lysates from 2 independent infections) was pooled for SYT-SSX2 ChIP.
2011-09-26 | E-GEOD-26564 | biostudies-arrayexpress
Project description:Synovial sarcoma is a rare malignancy that is characterized by the presence of a chromosomal translocation t(X;18). This genetic abnormality results in the fusion of 2 transcriptional co-regulators, SYT and SSX, which have been shown to mediate transcriptional activation and repression, respectively. Although the fusion protein does not bind DNA directly, SYT-SSX2 is known to function through interaction with chromatin-modifying complexes. In this study, we wanted to determine the SYT-SSX2 occupancy across the whole genome in order to further characterize its function by identifying genes that may be deregulated by this protein.
2011-09-26 | GSE26564 | GEO
Project description:Expression of the SS18/SYT-SSX fusion protein is believed to underlie the pathogenesis of synovial sarcoma (SS). Recent evidence suggests that deregulation of the Wnt pathway may play an important role in SS but the mechanisms whereby SS18-SSX might affect Wnt signaling remain to be elucidated. Here, we show that SS18/SSX tightly regulates the elevated expression of the key Wnt target AXIN2 in primary SS. SS18-SSX is shown to interact with TCF/LEF, TLE and HDAC but not β -catenin in vivo and to induce Wnt target gene expression by forming a complex containing promoter-bound TCF/LEF and HDAC but lacking β -catenin. Our observations provide a tumor-specific mechanistic basis for Wnt target gene induction in SS that can occur in the absence of Wnt ligand stimulation. SS18SSX expressing C3H cells vs control: no replicates. WNT-stimulated C3H cells vs controls: 3 replicates per condition
2016-02-23 | E-GEOD-78159 | biostudies-arrayexpress
Project description:Synovial sarcomas account for approximately 10% of all soft-tissue tumors and occur most frequently in young adults. A specific translocation in this sarcoma induces fusion of the SYT gene on chromosome 18 to the SSX genes on chromosome X, leading to proliferation of the tumor cells. The need for non-invasive biomarkers indicating recurrence and activity of this disease has sparked research into short non-coding RNA known as microRNA (miRNA). Patients and Methods: Serum samples of patients with active synovial sarcoma, healthy donors and leiomyosarcoma patients were collected. Cell-free serum was obtained by differential centrifugation steps and analyzed using an Affymetrix GeneChip miRNA Array v. 4.0. qRT-PCR was carried out to confirm a panel of miRNAs which where differentially expressed in the miRNA array.
2018-09-19 | E-MTAB-3888 | biostudies-arrayexpress