An integrative multi-platform analysis for biomarker discovery of osteosarcoma
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE14789 | GEO | 2011/09/16
SECONDARY ACCESSION(S): PRJNA112223
REPOSITORIES: GEO
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Project description:Three osteosarcoma (OS) cell lines (MG-63, Saos-2 and U-2 OS) and 1 osteoblastic cell line (hFOB1.19) were collected for this work. MG-63 was kindly provided by Dr. Agi Grigoriadis from University College London. Saos-2, U-2 OS and hFOB1.19 were purchased from ATCC. All cells used were kept in exponential phase of growth. Total RNA was extracted using the RNeasy Total RNA Isolation kit (QIAGEN). The quality and purity of the products were controlled by Agilent 2100. The final synthesized biotinylated cDNAs were hybridized to Affymetrix GeneChip® U133A 2.0 arrays following the protocol strictly. Arrays were scanned with the Affymetrix scanner 3000. Data analysis was performed by Microarray Suite 5.0 after pre-standard procedure. Link-test on datasets from both SELDI-TOF-MS and microarray high-throughput analysis platforms can accelerate the identification of tumor biomarkers. The results confirmed that CYC-1 with important biomedical function was an effective candidate biomarker for osteosarcoma early diagnosis.
2011-09-15 | E-GEOD-14789 | 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: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. Experiment Overall Design: This genome-wide analysis is the first study to utilize oligonucleotide array CGH to identify microaberrations in OS, likely to contain genes involved in OS tumor oncogenesis. A better understanding of the underlying molecular genetic events leading to tumor initiation and progression could result in the identification of prognostic markers and therapeutic targets.
2008-06-18 | E-GEOD-7077 | biostudies-arrayexpress
Project description:To establish a genomewide gene expression profile of OS-derived induced pluripotent stem cell lines (OS-iPSC): iG-292 and iSaos-2, against the parental cell lines, G-292 and Saos-2. OS cell lines were first reprogrammed into pluripotent state by retroviral transduction of OSKM. Six OS-iPSC clones and four parental OS cell lines were subjected to mRNA microarray analysis (Affymetrix Human PrimeView Chip).
2017-12-09 | GSE107855 | GEO
Project description:Osteosarcoma (OS) is the most prevalent primary malignant bone tumor.We have recently succeeded in generating CSC-like cells (MG-OKS) from the OS cell line MG-63 by transducing defined factors. A significant increase was observed in small proline-rich protein 1A (SPRR1A) expression, a cross-linked envelope protein in keratinocytes, in MG-OKS cells. This study aimed to evaluate the role of SPRR1A in OS using novel MG-OKS cells. MG-OKS cells were transfected with SPRR1A siRNA (siMG-OKS) to suppress SPRR1A expression selectively; MG-OKS and scrambled siRNA-transfected MG-OKS (scMG-OKS) cells served as controls. Our date that genes involved in cell adhesion were suppressed in the siMG-OKS group, suggesting that suppression of cell adhesion may cause phenotypic changes.
2024-11-01 | GSE268670 | GEO
Project description:To investigate whether IDO1 participated in OS malignant progression through miRNA, we selected non-metastatic OS cell line (MG63), metastatic OS cell line (143B) and non-tumorigenic immortalized osteoblastic hFOB1.19 cell line as the research object. Over Expression cell lines are contructed and exosomal miRNAs from both control and OE cell lines are sequenced to find out the differences in expression in the exosomes secreted from IDO1 overexpressing and WT cells.
2023-05-14 | GSE232452 | GEO
Project description:Osteosarcoma (OS) is an essential threatening tumor of bone in young adults. OS stem cells (OSCs) act a significant role in the occurrence, metastasis, drug resistance and recurrence of OS. CD133 is an integral membrane glycoprotein, which has been identified as an OSCs marker. However, the mechanisms of metastasis, chemoresistance and progression in CD133(+) OSCs need to be further explored. We aim to detect the lncRNA and mRNA profiles in CD133(+) cells compared with CD133(-) cells from the Saos-2 cell line in the present study.
2024-06-01 | GSE207333 | GEO
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: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:Whole testes were dissected from adult males. RNA from five or six biological replicates were generated and the expression profiles were determined using Affymetrix Drosophila Genechip 1 arrays. Comparisons between the bgcn- and Os+bgcn- groups allowed for the identification of stem cell genes. Keywords: repeat
2006-03-15 | GSE4188 | GEO