Schildgen, Verena, Pieper, Monika, Khalfaoui, Soumaya, Arnold, Wolfgang H. ORCID: 0000-0002-9335-1808 and Schildgen, Oliver ORCID: 0000-0003-4297-9627 (2018). Human Bocavirus Infection of Permanent Cells Differentiated to Air-Liquid Interface Cultures Activates Transcription of Pathways Involved in Tumorigenesis. Cancers, 10 (11). BASEL: MDPI. ISSN 2072-6694

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Abstract

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.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Schildgen, VerenaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Pieper, MonikaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Khalfaoui, SoumayaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Arnold, Wolfgang H.UNSPECIFIEDorcid.org/0000-0002-9335-1808UNSPECIFIED
Schildgen, OliverUNSPECIFIEDorcid.org/0000-0003-4297-9627UNSPECIFIED
URN: urn:nbn:de:hbz:38-166727
DOI: 10.3390/cancers10110410
Journal or Publication Title: Cancers
Volume: 10
Number: 11
Date: 2018
Publisher: MDPI
Place of Publication: BASEL
ISSN: 2072-6694
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
PARVOVIRUS INFECTION; VIRAL-INFECTIONS; MESSENGER-RNAS; TENASCIN-C; DNA; CANCER; SUSCEPTIBILITY; EXPRESSION; CHILDREN; REPAIRMultiple languages
OncologyMultiple languages
Refereed: Yes
URI: http://kups.ub.uni-koeln.de/id/eprint/16672

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