<HashMap><database>biostudies-arrayexpress</database><scores/><additional><omics_type>Metabolomics</omics_type><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><submitter>Huang Qingshan</submitter><study_type>transcription profiling by array</study_type><organism>Homo sapiens</organism><species>Homo sapiens</species><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-GEOD-76754</full_dataset_link><description>We superinfected a hepatocellular carcinoma (HCC) cell line (QGY-7703,QY) with oncolytic parvovirus H1 (H-1PV) and acquired a group of resistant cells QYRC. Previous studies suggested that cells surviving H-1PV superinfection should behave somewhat similarly to normal cells. When compared with the QGY-7703 cells, the QYRC cells indeed exhibited loss of colony formation in soft agar, and they didnâ&#x80;&#x99;t form detectable tumors after being hypodermically injected into 5 nude mice. In order to find out what cellular factors may be responsible for the loss of tumor cell phenotype, we compared the cDNA microarray profiles of the QGY-7703 and QYRC cells to find that a series of genes were upregulated in the H-1PV-resistant QYRC cells We investigated the expression profiles of QY and QYRC cell lines</description><repository>biostudies-arrayexpress</repository><sample_protocol>Scaning - GeneChips were scanned using the Hewlett-Packard GeneArray Scanner G2500A.</sample_protocol><sample_protocol>Hybridization - Following fragmentation, 10 ug of cRNA were hybridized for 16 hr at 45C on GeneChip Drosophila Genome Array. GeneChips were washed and stained in the Affymetrix Fluidics Station 400.</sample_protocol><sample_protocol>Nucleic Acid Extraction - Trizol extraction of total RNA was performed according to the manufacturer's instructions.</sample_protocol><sample_protocol>Labeling - Biotinylated cRNA were prepared according to the standard Affymetrix protocol from 6 ug total RNA (Expression Analysis Technical Manual, 2001, Affymetrix).</sample_protocol><figure_sub>MIAME Score</figure_sub><figure_sub>Raw Data</figure_sub><figure_sub>Organization</figure_sub><figure_sub>Assays and Data</figure_sub><figure_sub>Processed Data</figure_sub><figure_sub>MAGE-TAB Files</figure_sub><figure_sub>Array Designs</figure_sub><pubmed_authors>Jinjiang Huang</pubmed_authors><pubmed_authors>Huang Qingshan</pubmed_authors><pubmed_authors>Hongyu Wu</pubmed_authors><pubmed_authors>Kuikui Ge</pubmed_authors><pubmed_authors>Guodong Li</pubmed_authors><pubmed_authors>Qingshan Huang</pubmed_authors><pubmed_authors>Wei Wang</pubmed_authors><data_protocol>Data Transformation - The data were analyzed with Microarray Suite version 5.0 (MAS 5.0) using Affymetrix default analysis settings and global scaling as normalization method. The trimmed mean target intensity of each array was arbitrarily set to 100. ID_REF =  VALUE = MAS5.0 signal intensity ABS_CALL =  DETECTION P-VALUE =</data_protocol></additional><is_claimable>false</is_claimable><name>Expression data from QY and QYRC cell lines</name><description>We superinfected a hepatocellular carcinoma (HCC) cell line (QGY-7703,QY) with oncolytic parvovirus H1 (H-1PV) and acquired a group of resistant cells QYRC. Previous studies suggested that cells surviving H-1PV superinfection should behave somewhat similarly to normal cells. When compared with the QGY-7703 cells, the QYRC cells indeed exhibited loss of colony formation in soft agar, and they didnâ&#x80;&#x99;t form detectable tumors after being hypodermically injected into 5 nude mice. In order to find out what cellular factors may be responsible for the loss of tumor cell phenotype, we compared the cDNA microarray profiles of the QGY-7703 and QYRC cells to find that a series of genes were upregulated in the H-1PV-resistant QYRC cells We investigated the expression profiles of QY and QYRC cell lines</description><dates><release>2016-01-12T00:00:00Z</release><modification>2023-10-02T20:53:26.285Z</modification><creation>2022-03-07T01:38:10.497Z</creation></dates><accession>E-GEOD-76754</accession><cross_references><GEO>GSE76754</GEO><EFO>EFO_0002768</EFO></cross_references></HashMap>