Array-based comparative genomic hybridization for genomic-wide screening of DNA copy number alterations in aggressive bone tumors

Koike, Masahiko; Sano, Akimi; Yasuda, Taketoshi; Hori, Takeshi; Suzuki, Kayo

doi:10.1186/1756-9966-31-100

Cited by 19 publications

(19 citation statements)

References 20 publications

(22 reference statements)

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“…Spry2 protein is a good candidate to act as tumour suppressor in osteosarcoma. Corroborating with our data it is known that the q arm of chromosome 13 containing the SPRY2 gene frequently shows gene copy number losses in osteosarcoma [31,32]. Additionally it is shown that Spry2 expression interferes with ERK activation after FGF stimulation of osteoblasts [33].…”

Section: Discussionsupporting

confidence: 89%

Sprouty2 but not Sprouty4 is a potent inhibitor of cell proliferation and migration of osteosarcoma cells

et al. 2013

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a b s t r a c tAs negative regulators of receptor tyrosine kinase-mediated signalling, Sprouty proteins fulfil important roles during carcinogenesis. In this report, we demonstrate that Sprouty2 protein expression inhibits cell proliferation and migration in osteosarcoma-derived cells. Although earlier reports describe a tumour-promoting function, these results indicate that Sprouty proteins also have the potential to function as tumour suppressors in sarcoma. In contrast to Sprouty2, Sprouty4 expression failed to interfere with proliferation and migration of the osteosarcoma-derived cells, possibly due to a less pronounced interference with mitogen-activated protein kinase activity. Sequences within the NH 2 -terminus are responsible for the specific inhibitory function of Sprouty2 protein.

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Section: Discussionsupporting

confidence: 89%

Sprouty2 but not Sprouty4 is a potent inhibitor of cell proliferation and migration of osteosarcoma cells

et al. 2013

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“…Oligo aCGH has been applied to several human tumors, revealing a high degree of heterogeneity within similar histotypes, and recurrent regions of copy-number abnormalities in the tumoral genomic DNA led to the discovery of genes that drive disease pathogenesis [7]–[9], [11].…”

Section: Discussionmentioning

confidence: 99%

Array-Based Comparative Genomic Hybridization Analysis Reveals Chromosomal Copy Number Aberrations Associated with Clinical Outcome in Canine Diffuse Large B-Cell Lymphoma

et al. 2014

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Canine Diffuse Large B-cell Lymphoma (cDLBCL) is an aggressive cancer with variable clinical response. Despite recent attempts by gene expression profiling to identify the dog as a potential animal model for human DLBCL, this tumor remains biologically heterogeneous with no prognostic biomarkers to predict prognosis. The aim of this work was to identify copy number aberrations (CNAs) by high-resolution array comparative genomic hybridization (aCGH) in 12 dogs with newly diagnosed DLBCL. In a subset of these dogs, the genetic profiles at the end of therapy and at relapse were also assessed. In primary DLBCLs, 90 different genomic imbalances were counted, consisting of 46 gains and 44 losses. Two gains in chr13 were significantly correlated with clinical stage. In addition, specific regions of gains and losses were significantly associated to duration of remission. In primary DLBCLs, individual variability was found, however 14 recurrent CNAs (>30%) were identified. Losses involving IGK, IGL and IGH were always found, and gains along the length of chr13 and chr31 were often observed (>41%). In these segments, MYC, LDHB, HSF1, KIT and PDGFRα are annotated. At the end of therapy, dogs in remission showed four new CNAs, whereas three new CNAs were observed in dogs at relapse compared with the previous profiles. One ex novo CNA, involving TCR, was present in dogs in remission after therapy, possibly induced by the autologous vaccine. Overall, aCGH identified small CNAs associated with outcome, which, along with future expression studies, may reveal target genes relevant to cDLBCL.

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“…Five OS cell lines (HOS, MOS, MG-63, NOS-1 and HuO 9N2) were used in this study. The MOS and NOS-1 cell lines were kindly provided by Dr Masahiko Kanamori (School of Medicine, University of Toyama, Toyama, Japan) (32)(33)(34)(35)(36). Three cell lines (HOS, MG-63, and HuO 9N2) were obtained from the Japanese Collection of Research Bioresources cell bank (Ibaraki, Osaka, Japan).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of NADPH oxidase 2 induces apoptosis in osteosarcoma: The role of reactive oxygen species in cell proliferation

et al. 2018

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Abstract. Osteosarcomas (OS) are aggressive tumors that are characterized by dysregulated growth and resistance to apoptosis. Reactive oxygen species (ROS) are thought to be important signal transduction molecules in the regulation of cell growth. ROS-generating nicotinamide adenine dinucleotide phosphate oxidase (NOX) family enzymes have previously been suggested to be involved in neoplastic proliferation. To examine whether NOX-mediated generation of intracellular ROS confers anti-apoptotic activity, and thus a growth advantage, the current study first analyzed the mRNA expression of NOX family members by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) in five human OS cell lines. RT-PCR analysis revealed that NOX2 and NOX4 mRNAs were expressed in all the OS cell lines examined, whereas little or no NOX1 and NOX3 mRNAs were detected. By RT-qPCR, NOX2 mRNA expression levels were demonstrated to be higher than NOX4 mRNA expression levels. The viability of OS cells decreased in a dose-dependent manner with treatment of diphenylene iodonium (DPI), an inhibitor of flavoprotein-dependent oxidase. DPI treatment was observed to reduce intracellular ROS levels by ~50%, and increase the frequency of apoptosis by 30%. Notably, small interfering RNAs (siRNAs) targeting NOX2 significantly suppressed ROS generation; ROS depletion by DPI or NOX2 siRNAs induced apoptosis in OS cells. Together, the results of the present study indicate that NOX2-mediated ROS generation promotes cell survival and ROS depletion leads to apoptosis, thus highlighting the NOX2-ROS signaling pathway as a potential therapeutic target for OS treatment.

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Array-based comparative genomic hybridization for genomic-wide screening of DNA copy number alterations in aggressive bone tumors

Cited by 19 publications

References 20 publications

Sprouty2 but not Sprouty4 is a potent inhibitor of cell proliferation and migration of osteosarcoma cells

Sprouty2 but not Sprouty4 is a potent inhibitor of cell proliferation and migration of osteosarcoma cells

Array-Based Comparative Genomic Hybridization Analysis Reveals Chromosomal Copy Number Aberrations Associated with Clinical Outcome in Canine Diffuse Large B-Cell Lymphoma

Inhibition of NADPH oxidase 2 induces apoptosis in osteosarcoma: The role of reactive oxygen species in cell proliferation

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