Epstein-Barr virus circRNAome as host miRNA sponge regulates virus infection, cell cycle, and oncogenesis

References

• Young LS, Yap LF, Murray PG. Epstein-Barr virus: more than 50 years old and still providing surprises. Nat Rev Cancer. 2016;16(12):789–802.
   Google Scholar
• Rowlands DC, Ito M, Mangham DC, et al. Epstein-Barr virus and carcinomas: rare association of the virus with gastric adenocarcinomas. Br J Cancer. 2016;114(12):e15.
   Google Scholar
• Shannon-Lowe C, Rickinson AB, Bell AI. Epstein-Barr virus-associated lymphomas. Philos Trans R Soc Lond B Biol Sci. 2017;372:1732.
   Google Scholar
• Hsu JL, Glaser SL. Epstein-barr virus-associated malignancies: epidemiologic patterns and etiologic implications. Crit Rev Oncol Hematol. 2000;34(1):27–53.
   Google Scholar
• Tsao SW, Tsang CM, Lo KW. Epstein-Barr virus infection and nasopharyngeal carcinoma. Philos Trans R Soc Lond B Biol Sci. 2017;372:1732.
   Google Scholar
• Thompson MP, Kurzrock R. Epstein-Barr virus and cancer. Clin Cancer Res. 2004;10(3):803–821.
   Google Scholar
• Galetsky SA, Tsvetnov VV, Land CE, et al. Epstein-Barr-virus-associated gastric cancer in Russia. Int J Cancer. 1997;73(6):786–789.
   Google Scholar
• Dierickx D, Habermann TM. Post-transplantation lymphoproliferative disorders in adults. N Engl J Med. 2018;378(6):549–562.
   Google Scholar
• Dharnidharka VR, Webster AC, Martinez OM, et al. Post-transplant lymphoproliferative disorders. Nat Rev Dis Primers. 2016;2:15088.
   Google Scholar
• Yin H, Qu J, Peng Q, et al. Molecular mechanisms of EBV-driven cell cycle progression and oncogenesis. Med Microbiol Immunol. 2019;208(5):573–583.
   Google Scholar
• Toptan T, Abere B, Nalesnik MA, et al. Circular DNA tumor viruses make circular RNAs. Proc Natl Acad Sci U S A. 2018;115(37):E8737–E45.
   Google Scholar
• Ungerleider N, Concha M, Lin Z, et al. The Epstein Barr virus circRNAome. PLoS Pathog. 2018;14(8):e1007206.
   Google Scholar
• Rybak-Wolf A, Stottmeister C, Glazar P, et al. Circular RNAs in the mammalian brain are highly abundant, conserved, and dynamically expressed. Mol Cell. 2015;58(5):870–885.
   Google Scholar
• Jeck WR, Sorrentino JA, Wang K, et al. Circular RNAs are abundant, conserved, and associated with ALU repeats. RNA. 2013;19(2):141–157.
   Google Scholar
• Hansen TB, Jensen TI, Clausen BH, et al. Natural RNA circles function as efficient microRNA sponges. Nature. 2013;495(7441):384–388.
   Google Scholar
• Li Z, Huang C, Bao C, et al. Exon-intron circular RNAs regulate transcription in the nucleus. Nat Struct Mol Biol. 2015;22(3):256–264.
   Google Scholar
• Li X, Yang L, Chen LL. The biogenesis, functions, and challenges of circular RNAs. Mol Cell. 2018;71(3):428–442.
   Google Scholar
• Li LJ, Leng RX, Fan YG, et al. Translation of noncoding RNAs: focus on lncRNAs, pri-miRNAs, and circRNAs. Exp Cell Res. 2017;361(1):1–8.
   Google Scholar
• Pamudurti NR, Bartok O, Jens M, et al. Translation of circRNAs. Mol Cell. 2017;66(1):9–21 e7.
   Google Scholar
• Granados-Riveron JT, Aquino-Jarquin G. The complexity of the translation ability of circRNAs. Biochim Biophys Acta. 2016;1859(10):1245–1251.
   Google Scholar
• Hayes J, Peruzzi PP, Lawler S. MicroRNAs in cancer: biomarkers, functions and therapy. Trends Mol Med. 2014;20(8):460–469.
   Google Scholar
• Macfarlane LA, Murphy PR. MicroRNA: biogenesis, function and role in cancer. Curr Genomics. 2010;11(7):537–561.
   Google Scholar
• Liu W, Wang X. Prediction of functional microRNA targets by integrative modeling of microRNA binding and target expression data. Genome Biol. 2019;20(1):18.
   Google Scholar
• Wong N, Wang X. miRDB: an online resource for microRNA target prediction and functional annotations. Nucleic Acids Res. 2015;43(Databaseissue):D146–52.
   Google Scholar
• Panwar B, Omenn GS, Guan Y. miRmine: a database of human miRNA expression profiles. Bioinformatics. 2017;33(10):1554–1560.
   Google Scholar
• International Nucleotide Sequence Database C, Kodama Y, Shumway M, Leinonen R. The sequence read archive: explosive growth of sequencing data. Nucleic Acids Res. 2012;40(Databaseissue):D54–6.
   Google Scholar
• International Nucleotide Sequence Database C, Leinonen R, Sugawara H, Shumway M. The sequence read archive. Nucleic Acids Res. 2011;39(Databaseissue):D19–21.
   Google Scholar
• Fan Y, Siklenka K, Arora SK, et al. miRNet - dissecting miRNA-target interactions and functional associations through network-based visual analysis. Nucleic Acids Res. 2016;44(W1):W135–41.
   Google Scholar
• Chesnokova LS, Hutt-Fletcher LM. Epstein-Barr virus infection mechanisms. Chin J Cancer. 2014;33(11):545–548.
   Google Scholar
• Chen J, Sathiyamoorthy K, Zhang X, et al. Ephrin receptor A2 is a functional entry receptor for Epstein-Barr virus. Nat Microbiol. 2018;3(2):172–180.
   Google Scholar
• Chen J, Jardetzky TS, Longnecker R. The large groove found in the gH/gL structure is an important functional domain for Epstein-Barr virus fusion. J Virol. 2013;87(7):3620–3627.
   Google Scholar
• Polee MB, Kok TC, Siersema PD, et al. Phase II study of the combination cisplatin, etoposide, 5-fluorouracil and folinic acid in patients with advanced squamous cell carcinoma of the esophagus. Anticancer Drugs. 2001;12(6):513–517.
   Google Scholar
• Kok TC, Van der Gaast A, Dees J, et al. Cisplatin and etoposide in oesophageal cancer: a phase II study. rotterdam oesophageal tumour study group. Br J Cancer. 1996;74(6):980–984.
   Google Scholar
• Young RC. Etoposide in the treatment of non-Hodgkin’s lymphomas. Semin Oncol. 1992;19(6 Suppl 13):19–25.
   Google Scholar
• Comella P, Abate G, Di Finizio G, et al. Treatment of resistant non-Hodgkin’s lymphomas with cisplatin, etoposide, and bleomycin. Cancer Chemother Pharmacol. 1990;26(4):306–309.
   Google Scholar
• Sun G, Shi L, Yan S, et al. MiR-15b targets cyclin D1 to regulate proliferation and apoptosis in glioma cells. Biomed Res Int. 2014;2014:687826.
   Google Scholar
• Lovat F, Fassan M, Gasparini P, et al. miR-15b/16-2 deletion promotes B-cell malignancies. Proc Natl Acad Sci U S A. 2015;112(37):11636–11641.
   Google Scholar
• McCann JV, Xiao L, Kim DJ, et al. Endothelial miR-30c suppresses tumor growth via inhibition of TGF-beta-induced Serpine1. J Clin Invest. 2019;130:1654–1670.
   Google Scholar
• Kawaguchi T, Yan L, Qi Q, et al. Overexpression of suppressive microRNAs, miR-30a and miR-200c are associated with improved survival of breast cancer patients. Sci Rep. 2017;7(1):15945.
   Google Scholar
• Rodriguez-Barrueco R, Nekritz EA, Bertucci F, et al. miR-424(322)/503 is a breast cancer tumor suppressor whose loss promotes resistance to chemotherapy. Genes Dev. 2017;31(6):553–566.
   Google Scholar
• Thome M, Schneider P, Hofmann K, et al. Viral FLICE-inhibitory proteins (FLIPs) prevent apoptosis induced by death receptors. Nature. 1997;386(6624):517–521.
   Google Scholar
• Uemura N, Kajino T, Sanjo H, et al. TAK1 is a component of the Epstein-Barr virus LMP1 complex and is essential for activation of JNK but not of NF-kappaB. J Biol Chem. 2006;281(12):7863–7872.
   Google Scholar
• Tang S, Patel A, Krause PR. Herpes simplex virus ICP27 regulates alternative pre-mRNA polyadenylation and splicing in a sequence-dependent manner. Proc Natl Acad Sci U S A. 2016;113(43):12256–12261.
   Google Scholar
• Sciabica KS, Dai QJ, Sandri-Goldin RM. ICP27 interacts with SRPK1 to mediate HSV splicing inhibition by altering SR protein phosphorylation. Embo J. 2003;22(7):1608–1619.
   Google Scholar
• O’Connell D, Liang C. Autophagy interaction with herpes simplex virus type-1 infection. Autophagy. 2016;12(3):451–459.
   Google Scholar
• Lim S, Kaldis P. Cdks, cyclins and CKIs: roles beyond cell cycle regulation. Development. 2013;140(15):3079–3093.
   Google Scholar
• Nilsson I, Hoffmann I. Cell cycle regulation by the Cdc25 phosphatase family. Prog Cell Cycle Res. 2000;4:107–114.
   Google Scholar
• Qiu L, Wu J, Pan C, et al. Downregulation of CDC27 inhibits the proliferation of colorectal cancer cells via the accumulation of p21Cip1/Waf1. Cell Death Dis. 2016;7:e2074.
   Google Scholar
• Lei M. The MCM complex: its role in DNA replication and implications for cancer therapy. Curr Cancer Drug Targets. 2005;5(5):365–380.
   Google Scholar
• Hermeking H, Benzinger A. 14-3-3 proteins in cell cycle regulation. Semin Cancer Biol. 2006;16(3):183–192.
   Google Scholar
• Leone G, DeGregori J, Yan Z, et al. E2F3 activity is regulated during the cell cycle and is required for the induction of S phase. Genes Dev. 1998;12(14):2120–2130.
   Google Scholar
• Takahashi-Yanaga F, Sasaguri T. GSK-3beta regulates cyclin D1 expression: a new target for chemotherapy. Cell Signal. 2008;20(4):581–589.
   Google Scholar
• Zhang YF, Jiang R, Li JD, et al. SMC1A knockdown induces growth suppression of human lung adenocarcinoma cells through G1/S cell cycle phase arrest and apoptosis pathways in vitro. Oncol Lett. 2013;5(3):749–755.
   Google Scholar
• Sachs N, Secades P, van Hulst L, et al. Loss of integrin alpha3 prevents skin tumor formation by promoting epidermal turnover and depletion of slow-cycling cells. Proc Natl Acad Sci U S A. 2012;109(52):21468–21473.
   Google Scholar
• Kang HC, Wakabayashi Y, Jen KY, et al. Ptch1 overexpression drives skin carcinogenesis and developmental defects in K14Ptch(FVB) mice. J Invest Dermatol. 2013;133(5):1311–1320.
   Google Scholar
• Xu J, Fang Y, Wang X, et al. CUL2 overexpression driven by CUL2/E2F1/miR-424 regulatory loop promotes HPV16 E7 induced cervical carcinogenesis. Oncotarget. 2016;7(21):31520–31533.
   Google Scholar
• Hornsveld M, Dansen TB, Derksen PW, et al. Re-evaluating the role of FOXOs in cancer. Semin Cancer Biol. 2018;50:90–100.
   Google Scholar