Expression data from coculture of retinoblastoma (RB) and bone marrow stromal cells (BMSC)
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE130724 | GEO | 2019/12/11
REPOSITORIES: GEO
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Project description:Chemotherapy resistance is one of the reasons for the loss of the eye in retinoblastoma (RB) pa-tients. RB chemotherapy resistance has been investigated in different cell culture models like WERI RB1. Furthermore, chemotherapy resistant RB subclones like the etoposide resistant WERI ETOR cell line have been established to improve understanding of chemotherapy resistance in RB. Ob-jective of this study was to characterize the cell line models of an etoposide sensitive WERI RB1 and its etoposide resistant subclone WERI ETOR by proteomics analysis. Subsequently, quantitative proteomic data served for correlation analysis with known drug perturbation profiles. . WERI RB1 and WERI ETOR were cultured and prepared for quantitative mass spectrometry. Comparative proteomic profiling was performed with electrospray ionization tandem mass spectrometry in data-independent acquisition mode (SWATH). The raw SWATH files were processed using neural networks in library free mode along with machine learning algorithms. Pathway enrichment was performed using the REACTOME pathway resource and correlated to the Molecular Signature Database (MSigDB) hallmark gene set collections for functional annotation. Also, a drug connec-tivity analysis using the L1000 database was used to correlate the mechanism-of-action (MOA) for different anticancer reagents to WERI RB1 / WERI ETOR signatures. A total 4,756 proteins were identified across all samples which revealed a distinct clustering between groups. Of these pro-teins, 64 proteins were significantly altered (q < 0.05 & log2FC |>2|, 22% higher in WERI ETOR). Pathway analysis showed an enriched metabolic pathway for retinoid metabolism and transport pathway in WERI ETOR and for sphingolipid de novo biosynthesis in WERI RB1. In addition, this study showed similar protein signatures of topoisomerase inhibitors and WERI ETOR as well as of ATPase inhibitors, acetylcholine receptor antagonists and VEGFR inhibitors and WERI RB1. In this study, WERI RB1 and WERI ETOR were characterized as a cell line model for chemotherapy re-sistance in RB by using data-independent mass spectrometry. The global proteome revealed the activation of sphingolipid de novo biosynthesis in WERI RB1 and potential treatment options for etoposide resistant RB.
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Project description:Expression data from coculture of retinoblastoma (RB) and bone marrow stromal cells (BMSC)
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Project description:Retinoblastoma is a childhood retinal tumor that initiates in response to biallelic RB1 inactivation. We show that post-mitotic human cone precursors are uniquely sensitive to the oncogenic effects of Rb depletion. Rb knockdown induced cone precursor proliferation in prospectively isolated populations. SNP-array analysis of two Rb/p130-depleted cone precursor cell lines, revealing no megabase-size loss of heterozygosity (LOH) or copy number alterations (CNAs). SNP-array analysis of one Rb/p130-depleted (tumor 1) or one Rb-depleted (tumor 2) cone precursor-derived tumors, revealing no megabase-size LOH or CNAs, consistent with the lack of DNA copy number alterations in some retinoblastomas. Thus, the cone precursor tumors resembled human retinoblastomas at the molecular cytogenetic level. High resolution SNP-array DNA copy number analyses were performed using CytoScan® HD (Affymetrix, 901835) according to the manufacturer's directions. Data were analyzed using Chromosome Analysis Suite 2.0 (Affymetrix). DNA was extracted from two Rb/p130 depleted cone precursor cell lines and two cryopreserved mouse retinoblastoma samples from eyes xenograted with Rb/p130 or Rb depleted cone precursors. Affymetrix SNP analysis on retinoblastoma cell lines Y79, RB176, and WERI were used as control. Normal human genome 19 was used as reference.
2014-08-25 | E-GEOD-60720 | biostudies-arrayexpress
Project description:The main objective of the study is to identify the de-regulated miRNAs in association with HMGA2 (oncogene) in the Retinoblastoma tumorus. The present experiment was carried out using Y79 (Retinoblastoma cell line), as the invitro model of Retinoblastoma tumor. The HMGA2 transcripts were silenced using siRNA and the post-silenced RB cells (at the end of 48 hours) were subjected to miRNA profiling using agilent platform.The key miRNAs de-regulated in this experiment has been validated using qRT-PCR and further their role has been evaluated by addition of specific antagomirs in RB cell lines (Y79 and Weri Rb 1). Agilent one-color experiment,Organism: Homo sapiens ,Agilent Human miRNA 8x15k Arrays AMADID: 021827 [Agilent miRNA labeling reagent and Hybridization Kit Cat # 5190-0408] RB cells (Y79) treated with anti-HMGA2 siRNA or with control
2013-10-26 | E-GEOD-51696 | biostudies-arrayexpress
Project description:The main objective of the study is to identify the de-regulated miRNAs in association with HMGA2 (oncogene) in the Retinoblastoma tumorus. The present experiment was carried out using Y79 (Retinoblastoma cell line), as the invitro model of Retinoblastoma tumor. The HMGA2 transcripts were silenced using siRNA and the post-silenced RB cells (at the end of 48 hours) were subjected to miRNA profiling using agilent platform.The key miRNAs de-regulated in this experiment has been validated using qRT-PCR and further their role has been evaluated by addition of specific antagomirs in RB cell lines (Y79 and Weri Rb 1).
2013-10-26 | GSE51696 | GEO
Project description:carboplatin resistance retinoblastoma cell lines (Weri-RB1/CRP) transfect SNHG1-specific shSNHG1 to knockdown SNHG1 and analysis differential gene in Weri-RB1/CRP
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Project description:Fatty acid synthase is a major enzyme involved in de novo lipogenesis and associated with tumor invasion and poor prognosis. The effect of fatty acid synthase knockdown in retinoblastoma cancer cells (WERI RB1) using siRNA mediated gene silencing were accessed for global gene deregulations. The analysis resulted in RB cancer cell death through deregulations of various cell signalling, metabolic, immunity, angiogenesis, apoptosis and cell cycle pathway related genes. Further validations were done using qRT-PCR and western analysis. Our results provide evidence that blockade in lipid metabolism inturn lead to RB cancer cell death through impaired cell signalling pathway.
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Project description:Retinoblastoma (RB) is an intraocular childhood tumor which, if left untreated, leads to blindness and mortality. Nucleolin (NCL) protein which is differentially expressed on the tumor cell surface, binds ligands and regulates carcinogenesis and angiogenesis. We found that NCL is over expressed in RB tumor tissues and cell lines compared to normal retina. We studied the effect of nucleolin-aptamer (NCL-APT) to reduce proliferation in RB tumor cells. Aptamer treatment on the RB cell lines (Y79 and WERI-Rb1) led to significant inhibition of cell proliferation. Locked nucleic acid (LNA) modified NCL-APT administered subcutaneously (s.c.) near tumor or intraperitoneally (i.p.) in Y79 xenografted nude mice resulted in 26 and 65% of tumor growth inhibition, respectively. Downregulation of inhibitor of apoptosis proteins, tumor miRNA-18a, altered serum cytokines, and serum miRNA-18a levels were observed upon NCL-APT treatment. Desorption electrospray ionization mass spectrometry (DESI MS)-based imaging of cell lines and tumor tissues revealed changes in phosphatidylcholines levels upon treatment. Thus, our study provides proof of concept illustrating NCL-APT-based targeted therapeutic strategy and use of DESI MS-based lipid imaging in monitoring therapeutic responses in RB.
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Project description:Bone marrow stromal cells (BMSCs) can be expanded by serial passage, but expansion is limited by cell senescence. The nature of changes associated with BMSC serial passages was assessed. Transcriptome analysis of 10 early and 15 late passage samples from 5 subjects revealed 2193 differentially expressed genes; those highly expressed in early passage cells were overrepresented in skeletal system development, embryonic morphogenesis, tube morphogenesis, etc, while those highly expressed in the late passage BMSCs were overrepresented in nucleosome assembly; chromatin assembly, DNA packaging, etc. 57 BMSC samples from 7 donors were further analyzed for the transition from an early to late passage; 155 genes were highly correlated with BMSC senescence and a set of 24 genes was predictive of BMSCs lifespan. The change from an early to a late passage molecular signature occurred between passage 3 and 5. In contrast, senescence associated beta-galactosidase staining began to increase after passage 6 or 7 and colony formation efficiency began to fall after passage 7. These data indicated that the onset of molecular changes associated with BMSC passage varied among individuals and preceded changes in commonly used indicators of BMSC senescence. The set of 24 BMSC lifespan predictive genes will be useful in assessing the quality of clinical BMSC products.
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Project description:BMSC gene expression profiling was completed to examine the baseline neurotrophin and receptor gene expression in BMSC and to evaulate changes in gene expression in response to NGF or BDNF stimulation In the study, primary BMSC were treated with recombinant human NGF or BDNF for 24 hours. Following treatment, RNA isolated from the BMSC were analyzed using the Human Neurotrophin and Receptor Gene Array HS-018
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