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This article is part of the supplement: 15th International Conference on Human Retroviruses: HTLV and Related Viruses

Open Access Meeting abstract

Heme oxygenase-1 activation inhibits XMRV pathogenesis and carcinogenesis in prostate cancer cells

Subhash Dhawan

Author Affiliations

Laboratory of Molecular Virology, Division of Emerging and Transfusion Transmitted Diseases, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD, USA

Retrovirology 2011, 8(Suppl 1):A218  doi:10.1186/1742-4690-8-S1-A218


The electronic version of this article is the complete one and can be found online at: http://www.retrovirology.com/content/8/S1/A218


Published:6 June 2011

© 2011 Dhawan; licensee BioMed Central Ltd.

This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Meeting abstract

Heme oxygenase-1 (HO-1) induction by hemin, the active ingredient of an FDA-approved biologic for the treatment of acute porphyries, has been previously shown in our laboratory to effectively inhibit HIV-1 replication. The present study was undertaken to expand these observations to examine the inhibitory role of HO-1 in the pathogenesis of XMRV infection. Hemin-induced HO-1 activation in LNCaP, a prostate cancer cell line susceptible to XMRV infection, markedly down-modulated the cell surface expression of XMRV receptor Xpr1, and significantly inhibited their ability to support productive virus replication. Hemin treatment of XMRV-integrated prostate carcinoma cells 22Rv1 was relatively less effective in suppressing the rapidly replicating XMRV in these aggressive malignant cells; yet it efficiently inhibited XMRV infection of LNCaP cells by about 80% when cultured for three days in the virus-containing 50% conditioned media from 22Rv1 cells. Additionally, HO-1 induction retarded the growth of uninfected LNCaP cells, XMRV-infected LNCaP cells and 22Rv1 cells, and significantly reduced their invasiveness to the reconstituted basement membrane matrix Matrigel, consistent with the lower levels of basement membrane degrading enzyme matrix metalloproteinase-9. These findings indicate a pivotal role of HO-1 as a host cell defense mechanism in prostate carcinogenesis in vitro, and may offer HO-1 induction as a potentially novel therapeutic strategy to control the pathogenesis of XMRV infection.