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Cytomegalovirus infection blocks apoptosis in cancer cells.

Michaelis, Martin, Kotchetkov, Rouslan, Vogel, Jens-Uwe, Doerr, Hans Wilhelm, Cinatl, J. (2004) Cytomegalovirus infection blocks apoptosis in cancer cells. Cellular and Molecular Life Sciences, 61 (11). pp. 1307-16. ISSN 1420-9071. (doi:10.1007/s00018-004-3417-4) (The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided) (KAR id:34121)

The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided.
Official URL:
http://dx.doi.org/10.1007/s00018-004-3417-4

Abstract

Recent pathological findings reveal a higher frequency of human cytomegalovirus (HCMV) in tumor cells from different tumors compared with surrounding tissues. Experimental investigations suggest possible supportive effects of HCMV for tumor development and progression. One HCMV effect on tumor cells is the inhibition of apoptosis, leading to the promotion of tumor cell survival. Decreased sensitivity to treatment-induced tumor cell death is a major reason for failure of anticancer chemotherapy. HCMV infection interferes with both the intrinsic and extrinsic cellular apoptosis pathways. HCMV promotes cell survival signaling influencing the tumor suppressor p53 and its relative p73, and stimulates the antiapoptotic Ras/Raf/MEK/Erk- and PI-3K-signaling pathways. Antiapoptotic effects mediated by HCMV are inhibited by antiviral treatment in cell culture. Therefore, a better understanding of the influence of HCMV infection on tumor cell apoptosis might translate into improved anti-cancer therapy.

Item Type: Article
DOI/Identification number: 10.1007/s00018-004-3417-4
Subjects: Q Science > QR Microbiology > QR355 Virology
Divisions: Divisions > Division of Natural Sciences > Biosciences
Depositing User: Martin Michaelis
Date Deposited: 05 Jun 2013 20:15 UTC
Last Modified: 16 Nov 2021 10:11 UTC
Resource URI: https://kar.kent.ac.uk/id/eprint/34121 (The current URI for this page, for reference purposes)

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