Schildgen Verena, Pieper Monika, Khalfaoui Soumaya, Arnold Wolfgang H, Schildgen Oliver
Kliniken der Stadt Köln gGmbH, Institut für Pathologie, Kliniken der Privaten Universität Witten/Herdecke mit Sitz in Köln, Ostmerheimer Str. 200, D-51109 Köln/Cologne, Germany.
Universität Witten/Herdecke, Lehrstuhl für Biologische und Materialkundliche Grundlagen der Zahnmedizin, D-58448 Witten, Germany.
Cancers (Basel). 2018 Oct 30;10(11):410. doi: 10.3390/cancers10110410.
The parvoviral human bocavirus (HBoV) is a respiratory pathogen, able to persist in infected cells. The viral DNA has been identified in colorectal and lung tumors and thus it was postulated that the virus could be associated with tumorigenesis. This assumption was supported by the fact that in HBoV-infected patients and in an in vitro cell culture system, pro-cancerogenic and -fibrotic cytokines were expressed. In this work, it is shown by a whole transcriptome analysis that, also at the mRNA level, several pathways leading to neoplasia and tumorigenesis are significantly upregulated. In total, a set of 54 transcripts are specifically regulated by HBoV, of which the majority affects canonical pathways that may lead to tumor development if they become deregulated. Moreover, pathways leading to necrosis, apoptosis and cell death are downregulated, supporting the hypothesis that HBoV might contribute to the development of some kinds of cancer.
细小病毒属的人博卡病毒（HBoV）是一种呼吸道病原体，能够在受感染细胞中持续存在。在结直肠癌和肺癌肿瘤中已鉴定出病毒DNA，因此据推测该病毒可能与肿瘤发生有关。HBoV感染患者以及体外细胞培养系统中表达促癌和促纤维化细胞因子这一事实支持了这一假设。在这项研究中，全转录组分析表明，在mRNA水平上，几条导致瘤形成和肿瘤发生的途径也显著上调。总共有54个转录本受HBoV特异性调控，其中大多数影响经典途径，如果这些途径失调可能导致肿瘤发展。此外，导致坏死、凋亡和细胞死亡的途径下调，支持了HBoV可能促成某些类型癌症发生的假说。
