Academic Journal
The Oncogenic Effects, Pathways, and Target Molecules of JC Polyoma Virus T Antigen in Cancer Cells
العنوان: | The Oncogenic Effects, Pathways, and Target Molecules of JC Polyoma Virus T Antigen in Cancer Cells |
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المؤلفون: | Zheng, Hua-Chuan, Xue, Hang, Jin, Yu-Zi, Jiang, Hua-Mao, Cui, Zheng-Guo |
المصدر: | Frontiers in Oncology ; volume 12 ; ISSN 2234-943X |
بيانات النشر: | Frontiers Media SA |
سنة النشر: | 2022 |
المجموعة: | Frontiers (Publisher - via CrossRef) |
الوصف: | 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 2 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 transcriptionally targeted viral carcinogenesis, microRNAs in cancer, focal adhesion, p53, VEGF, phosphoinositide 3 kinase-Akt, and Forkhead box O signaling pathways, fructose and mannose metabolism, ribosome biosynthesis, and choline and pyrimidine metabolism. At a metabolomics level, it targeted protein digestion and absorption, aminoacryl-tRNA biosynthesis, biosynthesis of amino acids, and the AMPK signal pathway. At a proteomic level, it targeted ribosome biogenesis in eukaryotes, citrate cycle, carbon metabolism, protein digestion and absorption, aminoacryl-tRNA biosynthesis, extracellular-matrix-receptor interaction, and biosynthesis of amino acids. In lens tumor cells, T antigen might interact with various keratins, ribosomal proteins, apolipoproteins, G proteins, ubiquitin-related proteins, RPL19, β-catenin, β-TRCP, p53, and CCAAT-enhancer-binding proteins in lens tumor cells. T antigen induced a more aggressive phenotype in mouse and human cancer cells due to oncogene activation, inactivation of tumor suppressors, and disruption of metabolism, cell adhesion, and long noncoding RNA-microRNA-target axes. |
نوع الوثيقة: | article in journal/newspaper |
اللغة: | unknown |
DOI: | 10.3389/fonc.2022.744886 |
DOI: | 10.3389/fonc.2022.744886/full |
الاتاحة: | http://dx.doi.org/10.3389/fonc.2022.744886 https://www.frontiersin.org/articles/10.3389/fonc.2022.744886/full |
Rights: | https://creativecommons.org/licenses/by/4.0/ |
رقم الانضمام: | edsbas.9504F348 |
قاعدة البيانات: | BASE |
DOI: | 10.3389/fonc.2022.744886 |
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