<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>12</volume><submitter>Zheng HC</submitter><pubmed_abstract>JC polyoma virus (JCPyV) is a ubiquitous polyoma virus that infects the individual to cause progressive multifocal leukoencephalopathy and malignancies. Here, we found that T-antigen knockdown suppressed proliferation, glycolysis, mitochondrial respiration, migration, and invasion, and induced apoptosis and G&lt;sub>2&lt;/sub> arrest. The reverse was true for T-antigen overexpression, with overexpression of Akt, survivin, retinoblastoma protein, β-catenin, β-transducin repeat-containing protein (TRCP), and inhibitor of growth (ING)1, and the underexpression of mammalian target of rapamycin (mTOR), phosphorylated (p)-mTOR, p-p38, Cyclin D1, p21, vascular endothelial growth factor (VEGF), ING2, and ING4 in hepatocellular and pancreatic cancer cells and tissues. In lens tumor cells, T antigen trans</pubmed_abstract><journal>Frontiers in oncology</journal><pagination>744886</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8958009</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The Oncogenic Effects, Pathways, and Target Molecules of JC Polyoma Virus T Antigen in Cancer Cells.</pubmed_title><pmcid>PMC8958009</pmcid><pubmed_authors>Jin YZ</pubmed_authors><pubmed_authors>Jiang HM</pubmed_authors><pubmed_authors>Zheng HC</pubmed_authors><pubmed_authors>Cui ZG</pubmed_authors><pubmed_authors>Xue H</pubmed_authors></additional><is_claimable>false</is_claimable><name>The Oncogenic Effects, Pathways, and Target Molecules of JC Polyoma Virus T Antigen in Cancer Cells.</name><description>JC polyoma virus (JCPyV) is a ubiquitous polyoma virus that infects the individual to cause progressive multifocal leukoencephalopathy and malignancies. Here, we found that T-antigen knockdown suppressed proliferation, glycolysis, mitochondrial respiration, migration, and invasion, and induced apoptosis and G&lt;sub>2&lt;/sub> arrest. The reverse was true for T-antigen overexpression, with overexpression of Akt, survivin, retinoblastoma protein, β-catenin, β-transducin repeat-containing protein (TRCP), and inhibitor of growth (ING)1, and the underexpression of mammalian target of rapamycin (mTOR), phosphorylated (p)-mTOR, p-p38, Cyclin D1, p21, vascular endothelial growth factor (VEGF), ING2, and ING4 in hepatocellular and pancreatic cancer cells and tissues. In lens tumor cells, T antigen trans</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-19T22:12:29.667Z</modification><creation>2025-04-19T22:12:29.667Z</creation></dates><accession>S-EPMC8958009</accession><cross_references><pubmed>35350574</pubmed><doi>10.3389/fonc.2022.744886</doi></cross_references></HashMap>