Unknown,Transcriptomics,Genomics,Proteomics

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Affymetrix SNP array data for DNA copy number analysis of supernatant DNA

ABSTRACT: DNA contained in the supernatant of cultured malignant cells as well as from plasma/serum of cancer patients is able to transform recipient immortal murine NIH3T3 cells. We demonstrate for the first time that human circulating DNA is able to drive tumor progression in an immunocompetent colon carcinogenesis rat model and that treatment with DNAse I/proteases has antitumor effects in a xenograft nude mice model. DNA copy number analysis of the DNA purifed from the supernatat of SW480 cell cultures was analyzed to determine if specific regions of the genome are represented in this fraction. We hybridized genomic DNA from parental SW480 cells, the DNA isolated from supernatant of SW480 cells, onto the 500K Affymetrix genotyping array set, following the manufacturer´s instructions, and compared their DNA copy number profile against a common reference generated using data from the International HapMap project.

ORGANISM(S): Homo sapiens

SUBMITTER: Alfredo Hidalgo-Miranda

PROVIDER: E-GEOD-35052 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Chromosomal DNA copy number alterations are a hallmark of human malignancies, including hepatocellular carcinoma (HCC). However, which oncogenes or tumor suppressors located on regions with DNA copy number aberration may contribute to HCC initiation and progression still remain obscure. Here we performed a genome-wide DNA copy number analysis on human HCC samples to identify novel potential oncogenes or tumor suppressors with DNA copy number aberrations. Genome-wide DNA copy numbers analysis was performed with single nucleotide polymorphism micoarray. RT-PCR and immunohistochemical staining were employed to evaluate the NOXIN expression in HCC samples. Colony formation, cell cycle analysis and tumor xenograft assays were performed to assess the role of NOXIN in HCC cells. Reciprocal co-immunoprecipitation experiments were used to detect the interaction between NOXIN and DNA polymerase a primase. Genome-wide DNA copy number analysis on 43 paired HCC samples indentified the smallest DNA amplification region containing NOXIN, along with the elevated transcript. NOXIN overexpression was significantly associated with HCC tumor stage. Enforced NOXIN promoted cellular proliferation, colony formation, cell migration and in vivo tumorigenicity, whereas RNA interference against NOXIN can attenuate these effects. Interestingly, NOXIN overexpression can accelerate the G1-S transition of cell cycle progression through enhancing DNA synthesis in HCC cells, as indicated by bromodeoxyuridine incorporation. Furthermore, NOXIN can interact with DNA polymerase a, implying that NOXIN may promote de novo DNA synthesis via affiliating formation of DNA polymerase-primase complex. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from hepatocellular carcinoma and adjacent liver tissue samples. Copy number analysis of Affymetrix 500K SNP arrays was performed for 43 hepatocellular carcinoma tissue samples, which their adjacent liver tissues were used as references for copy number inference.

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Affymetrix SNP array data for DNA copy number analysis of supernatant DNA

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