RUNX2 and CBFB genome-wide binding in osteosarcoma SAOS2 cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE76937 | GEO | 2017/02/11
SECONDARY ACCESSION(S): PRJNA309084
REPOSITORIES: GEO
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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
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:The goal is to identify transcripts that are regulated by RUNX2 in SAOS2 cells.
2017-02-11 | GSE77352 | GEO
Project description:RUNX2 and CBFB genome-wide binding in osteosarcoma SAOS2 cells
| PRJNA309084 | ENA
Project description:Investigation of the transcriptional consequences of RUNX2 and CBFB loss in the presence and absence of the MEK inhibitor selumetinib in LoVo ERN1 knockout KRAS mutant colorectal cancer cells.
2019-10-22 | GSE139169 | GEO
Project description:Osteosarcoma is the most common primary malignant bone tumor with a high risk of metastasis and recurrence. Metabolic reprogramming is a hallmark of osteosarcoma and other cancers and is associated with genetic and epigenetic alterations. RUNX2 is an important transcription factor for osteoblastic differentiation, and aberrant expression of the gene contributes to the development and progression of osteosarcoma. To identify the effects of RUNX2 silencing on transcriptomic and metabolomic profiles in osteosarcomas, we generated SJSA-1 osteosarcoma cells stably expressing RUNX2 shRNA and SJSA-1 cells stably expressing scramble shRNA and analyzed transcriptome and metabolome profiles in the two cell types using Illumina NovaSeq 6000 and ultrahigh-performance liquid chromatography coupled with time-of-flight mass spectrometry, respectively. The datasets can be used by researchers to identify novel targets of RUNX2 and elucidate the role and underlying mechanism of RUNX2 in osteosarcoma pathogenesis and metabolic reprogramming.
2023-06-25 | GSE158976 | GEO
Project description:Ror2 is a member of the Ror-family of receptor tyrosine kinases acting as a receptor for Wnt5a. Wnt5a/Ror2 signaling activates primarily the ß-catenin-independent pathway, which involves various signal mediators, such as Dishevelled, c-Jun N-terminal kinase (JNK), filamin A, c-Src, and Ca2+. Wnt5a/Ror2 signaling has also been shown to inhibit the ß-catenin-dependent pathway. Wnt5a and Ror2 are overexpressed in various types of tumor cells, including osteosarcoma and melanoma cells, resulting in constitutive activation of Wnt5a/Ror2 signaling in a cell-autonomous manner. Constitutively activated Wnt5a/Ror2 signaling has been shown to play important roles in promoting invadopodia formation and invasiveness of tumor cells. However, little is known about the mechanisms underlying these processes. As an attempt to understand the mechanism by which Wnt5a/Ror2 signaling, activated constitutively in osteosarcoma cells, contributes to their highly invasive properties, we performed DNA microarray analysis using a human osteosarcoma cell line, SaOS2.
2017-01-01 | GSE76535 | GEO
Project description:Analysis of common pediatric osteosarcoma cell lines SaOS2, U2OS and 143B and two patient derived xenograft samples in comparison of osteoblast cell line hFOB1.19.
2022-02-22 | GSE197158 | GEO
Project description:Osteosarcoma is the most common bone sarcoma in children and young adults. While chemotherapy is universally delivered, benefit from chemotherapy is limited to roughly half of localized patients. Increasingly, intratumoral heterogeneity is being appreciated as a source of therapeutic resistance. In this study we developed and evaluated an in vitro model of osteosarcoma heterogeneity, characterizing phenotype (growth in varying environments, sensitivity to chemotherapy) and genotype. We present the genotypic and phenotypic characterization of an osteosarcoma cell line panel with a focus on coculture of the most phenotypically divergent cell lines, 143B and SAOS2. The extent of phenotypic heterogeneity can be altered with relatively modest environmental (pH, glutamine) or chemical perturbations. We demonstrate that in nutrient rich in vitro culture conditions 143B outcompetes SAOS2, but with selection pressure from nutrient variations or conventional chemotherapy, SAOS2 growth can be favored in spheroids. Importantly, perturbations that affect the faster growing cell line have only a modest effect on final spheroid size when the simplest heterogeneity state (a two-cell line coculture) is evaluated, and thus the only evaluated therapies to eliminate the spheroids were by switching therapies from a first strike to a second strike. This extensively characterized, widely available system can be modeled and scaled to allow for improved strategies to anticipate resistance in osteosarcoma due to phenotypic heterogeneity.
2023-11-22 | GSE240278 | GEO
Project description:RNA immunoprecipitation assay followed by next generation sequencing (RIPseq) to identify RNAs bound by CBFB and hnRNPK in breast cells.
2019-04-18 | GSE119800 | GEO