Affymetrix CytoscanHD data for genomic plasticity of osteosarcoma cell lines
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE67125 | GEO | 2015/05/01
SECONDARY ACCESSION(S): PRJNA279006
REPOSITORIES: GEO
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Project description:To identify chromosomal aberrations during passaging of parental SAOS-2 osteosarcoma cells with low metastatic potential and of SAOS-2-derived LM5 cells with increased metastatic potential DNA of early and late passage SAOS-2 and LM5 cells was analyzed by Affymetrix Cytoscan HD genotyping arrays
2015-05-01 | E-GEOD-67125 | biostudies-arrayexpress
Project description:To identify the genes that are regulated during passaging of the parental osteosarcoma cells SAOS-2 and HOS with low metastatic potential, and SAOS-2-derived LM5 cells and Ki-ras transformed HOS cells (143B) with increased metastatic potential, we performed global gene expression profiling in early and late passage cells.
2015-03-10 | GSE66673 | GEO
Project description:Osteosarcoma (OS) is the most common primary malignant tumor of bone; it occurs most commonly in the metaphyseal regions of long bones in adolescents and young adults. Conventional osteosarcoma is characterized by complex karyotypes with a high degree of aneuploidy and numerous structural aberrations such as copy number alterations (CNAs) and genomic rearrangements. The data comprise of array copy number data (N=113) from pre-therapeutic osteosarcoma. These have been derived from Affymetrix CytoscanHD. The study searches for driver genes and examines cancer evolution. Note (added 8th June 2016): This experiment is extended in an experiment described under accession E-MTAB-4815. It contains data for 97 samples from this experiment are also included in E-MTAB-4815.
2015-11-09 | E-MTAB-3998 | biostudies-arrayexpress
Project description:To identify the genes that are regulated during passaging of the parental mouse Dunn osteosarcoma cells with low metastatic potential and Dunn-derived LM8 cells with increased metastatic potential, we performed global gene expression profiling in early and late passage cells.
2015-03-10 | GSE66674 | GEO
Project description:Background Osteosarcoma (OS) is the most common malignant bone tumor in children and adolescents. The survival rate of patients with metastatic disease remains very dismal. Nevertheless, metastasis is a complex process and a single-level analysis is not likely to identify its key biological determinants. In this study, we used a systems biology approach to identify common metastatic pathways that are jointly supported by both mRNA and protein expression data in two distinct human metastatic OS models. Results mRNA expression microarray and N-linked glycoproteomic analyses were performed on two commonly used isogenic pairs of human metastatic OS cell lines, namely HOS/143B and SaOS-2/LM7. Pathway analysis of the differentially regulated genes and glycoproteins separately revealed pathways associated to metastasis including cell cycle regulation, immune response, and epithelial-to-mesenchymal-transition. However, no common significant pathway was found at both genomic and proteomic levels between the two metastatic models, suggesting a very different biological nature of the cell lines. To address this issue, we used a topological significance analysis based on a “shortest path” algorithm to identify topological nodes, which uncovered additional biological information with respect to the genomic and glycoproteomic profiles but remained hidden from the direct analyses. Pathway analysis of the significant topological nodes revealed a striking concordance between the models and identified significant common pathways, including “Cytoskeleton remodeling/TGF/WNT”, “Cytoskeleton remodeling/Cytoskeleton remodeling”, and “Cell adhesion/Chemokines and adhesion”. Of these, the “Cytoskeleton remodeling/TGF/WNT” was the top ranked common pathway from the topological analysis of the genomic and proteomic profiles in the two metastatic models. The up-regulation of proteins in the “Cytoskeleton remodeling/TGF/WNT” pathway in the SaOS-2/LM7 and HOS/143B models was further validated using an orthogonal Reverse Phase Protein Array platform. Conclusions In this study, we used a systems biology approach by integrating genomic and proteomic data to identify key and common metastatic mechanisms in OS. The use of the topological analysis revealed hidden biological pathways that are known to play critical roles in metastasis. Wnt signaling has been previously implicated in OS and other tumors, and inhibitors of Wnt signaling pathways are available for clinical testing. Further characterization of this common pathway and other topological pathways identified from this study may lead to a novel therapeutic strategy for the treatment of metastatic OS. In this study we analyzed two human metastatic OS cell lines and their parental non-metastatic lines. The two human metastatic OS cell line models were HOS/143B and SaOS-2/LM7. The HOS cell line, originally known as M.T. and later as TE-85, was derived from an OS of a 13 year-old girl. The 143B metastatic subline was generated from HOS by a Ki-RAS oncogene transformation [Rhim, J.S., et al., Characterization of human cells transformed in vitro by N-methyl-N'-nitro-N-nitrosoguanidine. Int J Cancer, 1977. 19(4): p. 505-10.]. The SaOS-2 cell was derived from an OS of an 11 year-old girl, and its metastatic subline LM7, was developed by multiple in vivo selection of SaOS-2 cells in mice with pulmonary metastases [Jia, S.F., L.L. Worth, and E.S. Kleinerman, A nude mouse model of human osteosarcoma lung metastases for evaluating new therapeutic strategies. Clin Exp Metastasis, 1999. 17(6): p. 501-6.]. No replicates were included.
2012-04-24 | E-GEOD-37552 | biostudies-arrayexpress
Project description:Background: Osteosarcoma (OS) is a very aggressive bone tumor characterized by highly abnormal complex karyotypes. With the improved resolution offered by array comparative genomic hybridization (array CGH) platforms, it is possible to readily detect cryptic microaberrations in genomic DNA. The identification of these microaberrations in genetic syndromes is currently the focus of many array CGH studies, but there have been no analyses to date documenting the occurrence of microaberrations in tumors. Results: In this study we utilized high-resolution oligonucleotide array CGH to identify novel microaberrations under ~750 kb in four OS-derived cell lines: U-2 OS, HOS, MG-63 and SAOS-2. Comparative analysis of these alterations showed that SAOS-2 harbored the most microaberrations at 17, followed by MG-63 with 11, HOS with 9 and U-2 OS with 6. SAOS-2, which has a TP53 mutation, exhibited the highest level of chromosomal instability in previous studies by our group; whereas U-2 OS, which has wild-type p53 status, exhibited the least instability. A consensus region of gain at 5p15.33 was detected in three of the four OS-derived cell lines (HOS, MG-63 and SAOS-2) by aCGH. Of these consensus gains, one was a microaberration of 500 kb in SAOS-2, and confirmed by fluorescence in situ hybridization analysis. It should be noted that this microaberration is immediately telomeric to the TERT gene, which also showed gain. TERT is correlated with increased tumor aggression, as well as decreased progression free survival in OS patients. Keywords: comparative genomic hybridization (array CGH)
2007-12-31 | GSE7077 | GEO
Project description:Osteosarcoma is the most common primary bone sarcoma. About 50% of patients develop metastatic disease and their 5-year survival lingers at around 20-30%. T cell checkpoint blockade immunotherapies have revolutionized cancer treatment in the last decade, but their impact remains limited in osteosarcoma. In order to reveal potentially novel immunotherapeutic strategies for advanced osteosarcoma, we conducted an immunogenomic characterization of a unique sample set comprising multiple osteosarcoma samples from seven patients, collected throughout the progression of the disease. We performed RNA-sequencing and imaging mass cytometry analysis on those samples to reveal the immunological landscape during osteosarcoma progression. Transcriptional and phenotypical hallmarks of cytotoxic T cell-driven anti-cancer immunity were enriched in metastatic lesions as compared to primary tumors. In parallel, we found a pronounced increase in the expression of cancer testis antigens, particularly MAGEA-related antigens, in osteosarcoma metastases. Their overexpression in metastatic lesions was confirmed at protein level and positive expression of MAGEA3 in primary tumors showed a significant association with metastasis free survival. Importantly, we demonstrated the presentation of MAGE-derived peptides in three osteosarcoma cell lines. These findings indicate a concurrent augmentation of cytotoxic anti-tumor immune responses and expression of MAGEA antigens from primary to metastatic osteosarcoma. This observation warrants the exploration of MAGEA antigens as potential targets for immunotherapy in the treatment of advanced osteosarcoma.
2024-02-07 | GSE237033 | GEO
Project description:Lobaplatin is a third-generation platinum-based antineoplastic agent and is widely used for osteosarcoma treatment before and after tumor removal. However, treatment failure often results from lobaplatin drug resistance. In our study, we found that SaOS-2 and SOSP-9607 osteosarcoma cells became less sensitive to lobaplatin after treatment with exogenous interleukin (IL)-6. Quantitative proteomic analysis was performed to elucidate the underlying mechanism in SaOS-2 osteosarcoma cells. Cells were divided into a control group (CG), a lobaplatin treatment group (LG) and a recombinant human IL-6 (rhIL-6) and lobaplatin group (rhILG). We performed three biological replicates in each group to compare the differential protein expression between groups using tandem mass tag (TMT) labeling technology based on liquid chromatography–tandem mass spectrometry (LC-MS/MS). A total of 1,313 proteins with significantly differential expression were identified and quantified. The general characterizations of significantly enriched proteins were identified by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, and protein-protein interaction (PPI) analysis was conducted using IntAct and STRING. In total, 31 proteins were further verified by parallel reaction monitoring (PRM), in which Ras GTPase-activating protein-binding protein 1 (G3BP1), fragile X mental retardation syndrome-related protein 1 (hFXR1p) and far upstream element-binding protein 1 (FUBP1) were significantly differentially expressed. Immunohistochemistry results showed that these three proteins are highly expressed in specimens of platinum-resistant osteosarcoma patients, while the proteins are negatively or weakly expressed in specimens of platinum-sensitive osteosarcoma patients. The results of immunofluorescence staining were in accordance with those of immunohistochemistry staining. This is the first proteomic study on rhIL-6 intervention before lobaplatin treatment in osteosarcoma cells.
2021-02-25 | PXD021564 | Pride
Project description:SaOS2 osteosarcoma cells were cultured with or without atorvastatin (10 µM) for 6, 15 or 24h (2 biological replcates). RNA were isolated and hybridized to RNG microarrays. Background Osteosarcoma is the most common primary tumor of bone. The rapid development of metastatic lesions and resistance to chemotherapy remain major mechanisms responsible for the failure of treatments and poor survival rate for patients. Methods We previously showed that the HMGCoA reductase inhibitors statins exhibit anti-tumoral effects on osteosarcoma cells. Here, using microarray analysis, we identify cyr61/CCN1 as a new target of statins. Modulations of expression of cyr61 were performed in human and murine osteosarcoma cell lines to investigate in vitro cell viability, migratory potential and invasiveness. Cyr61 expression was evaluated in 231 tissue cores from osteosarcoma patients using tissue microarray. Tumor behavior and metastases occurence were analysed by IM injection of modified osteosarcoma cells to BALB/c mice. Results Transcriptome comparisons revealed that statins down-regulate cyr61 expression in SaOS2 cells. Cyr61 silencing in human and murine osteosarcoma cell lines enhanced cell death, but reduced cell migration and cell invasion compared to parental cells whereas cyr61 overexpression had opposite effects. Tissue microarray analysis demonstrated that cyr61 protein expression is higher in human osteosarcoma compared to normal bone tissue and is further increased in metastatic tissues. In vivo, cyr61 overexpression in osteosarcoma cells enhanced lung metastases development whereas cyr61 silencing strongly reduced metastases in mice. Conclusion The results reveal that cyr61 expression increases with tumor grade in human osteosarcoma and demonstrate that cyr61 silencing inhibits in vitro osteosarcoma cell invasion and migration as well as in vivo lung metastases in mice. These data provide a novel molecular target for therapeutic intervention in metastatic osteosarcoma. Dye balance-experiment comparing atorvastatin versus untreated cells at 6, 15 and 24 hours using 2 biological replicates.
2011-02-22 | E-GEOD-24401 | biostudies-arrayexpress
Project description:SaOS2 osteosarcoma cells were cultured with or without atorvastatin (10 µM) for 6, 15 or 24h (2 biological replcates). RNA were isolated and hybridized to RNG microarrays. Background Osteosarcoma is the most common primary tumor of bone. The rapid development of metastatic lesions and resistance to chemotherapy remain major mechanisms responsible for the failure of treatments and poor survival rate for patients. Methods We previously showed that the HMGCoA reductase inhibitors statins exhibit anti-tumoral effects on osteosarcoma cells. Here, using microarray analysis, we identify cyr61/CCN1 as a new target of statins. Modulations of expression of cyr61 were performed in human and murine osteosarcoma cell lines to investigate in vitro cell viability, migratory potential and invasiveness. Cyr61 expression was evaluated in 231 tissue cores from osteosarcoma patients using tissue microarray. Tumor behavior and metastases occurence were analysed by IM injection of modified osteosarcoma cells to BALB/c mice. Results Transcriptome comparisons revealed that statins down-regulate cyr61 expression in SaOS2 cells. Cyr61 silencing in human and murine osteosarcoma cell lines enhanced cell death, but reduced cell migration and cell invasion compared to parental cells whereas cyr61 overexpression had opposite effects. Tissue microarray analysis demonstrated that cyr61 protein expression is higher in human osteosarcoma compared to normal bone tissue and is further increased in metastatic tissues. In vivo, cyr61 overexpression in osteosarcoma cells enhanced lung metastases development whereas cyr61 silencing strongly reduced metastases in mice. Conclusion The results reveal that cyr61 expression increases with tumor grade in human osteosarcoma and demonstrate that cyr61 silencing inhibits in vitro osteosarcoma cell invasion and migration as well as in vivo lung metastases in mice. These data provide a novel molecular target for therapeutic intervention in metastatic osteosarcoma.
2011-02-22 | GSE24401 | GEO