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Mammalian Orthoreovirus (MRV), a double-stranded RNA virus, is a potent oncolytic virus, which specifically replicates in tumor cells and consequently kills them. Hypoxia, a condition of low oxygen, is a characteristic feature of most solid tumors and develops due to tumor cells outgrowing their blood supply. Hypoxic cell survival is driven by the transcriptional activity of hypoxia inducible factor-1 (HIF-1). We examined the ability of MRV to infect hypoxic prostate tumor cells and found that not only did it successfully translate proteins and replicate in hypoxic prostate tumor cells, it also induced apoptosis. In addition, MRV induced downregulation of the HIF-1α protein, through a ubiquitin-dependent proteasome-mediated pathway, required the PAS domain of HIF-1α and was rescued by knockdown of the Receptor for Activated C Kinase 1 (RACK1). We investigated the direct involvement of any MRV proteins in the downregulation of HIF-1α and found that proteins μ1 and μ2 were able to downregulate HIF-1α independently. Strain specific difference (specifically the aa at 208 position of the protein) was found to affect the ability of μ2 to induce downregulation of HIF-1α; the T1L and T3D causing more downregulation than the T3D MRV strains. The region of μ2 containing aa 188-380 and the φ domain of μ1 were determined to be needed for HIF1α downregulation. The dependence of Prostate Cancer (PCa) on androgens for growth and survival is exploited by the hormone therapy, where androgen deprivation is used as a viable

Molecular effects of Mammalian Orthoreovirus (MRV) infection on hypoxic prostate tumor cells