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. 2018 Aug 22;8:12574. doi: 10.1038/s41598-018-30109-1

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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The transcriptome of HMECs infected with HCMV-DB displays oncogenic traits. (A) Upregulation of the gene expression of oncogenes: Myc (MYC), Fos (FOS), Jun (JUN), KRas (KRAS), HRas (HRAS) and NRas (NRAS), (B) Upregulation of the gene expression of tumor suppressor genes: TP53, TP73, FHIT, VHL, SMAD4, TGFB1, STK11, TSC1, RB1. (C) Expression of genes from the IL-6/JAK-STAT3 axis. (D) Left panel, Upregulation of genes coding for the cyclins: CCNA1, CCNA2, CCND1, CCNE1 and the cyclin dependent kinase 4 CDK4. Right panel, Upregulation of genes coding for the cyclin dependent kinase inhibitors: CDKN 1 A, CDKN 2 A, CDKN 2B and CDKN 3. (E) Upregulation of the expression of genes coding for proliferation markers, the Ki67 antigen (MKI67) and the topoisomerase 2 (TOPO2A). (F) Upregulation of the expression of genes involved in cell survival (NFKB1, REL, AKT1, PIK3C2A, BCL-2) and downregulation of the expression of caspase 8 (CASP8). (G) Downregulation of gene expression of the members of the MAPK cascade (MAPK3, MAPK8, MOS, GLI1, IGF1R). (H) Upregulation of the expression of genes involved in DNA reparation: the ataxia telangiectasia mutated (ATM) and human MutL homolog (MLH1). The up- and down-regulation were measured in HMECs infected with HCMV-DB (moi, 1 and 10) as compared to uninfected HMECs.