Apoptosis Induced by Mammalian Reovirus Is Beta Interferon (IFN) Independent and Enhanced by IFN Regulatory Factor 3- and NF-κB-Dependent Expression of Noxa

Knowlton, Jonathan J.; Dermody, Terence S.; Holm, Geoffrey H.

doi:10.1128/jvi.05924-11

Cited by 46 publications

(38 citation statements)

References 91 publications

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“…The cytochome c was released into cytosol and then leaded to cell apoptosis [14,15]. In mammalians, Noxa protein plays an important role in apoptosis induced by mammalian reovirus [16,17]. In zebrafish, Noxa protein was a key mediator of apoptosis in both embryogenesis and adult [18,19].…”

Section: Introductionmentioning

confidence: 99%

Expression pattern and transcriptional regulatory mechanism of noxa gene in grass carp (Ctenopharyngodon idella)

Pei

Lü

et al. 2015

Fish & Shellfish Immunology

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Section: Introductionmentioning

confidence: 99%

Expression pattern and transcriptional regulatory mechanism of noxa gene in grass carp (Ctenopharyngodon idella)

Pei

Lü

et al. 2015

Fish & Shellfish Immunology

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“…It has been reported that reoviral oncolysis is beta interferon independent and is enhanced by interferon regulatory factor 3 and NF-κB-dependent expression of Noxa, a protein that promotes activation of caspases and apoptosis [8]. Activation of caspase 3 has also been reported to be necessary for development of reovirus induced encephalitis [9].…”

Section: Introductionmentioning

confidence: 99%

Oncolytic reovirus preferentially induces apoptosis in KRAS mutant colorectal cancer cells, and synergizes with irinotecan

et al. 2014

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Reovirus is a double stranded RNA virus, with an intrinsic preference for replication in KRAS mutant cells. As 45% of human colorectal cancers (CRC) harbor KRAS mutations, we sought to investigate its efficacy in KRAS mutant CRC cells, and examine its impact in combination with the topoisimerase-1 inhibitor, irinotecan. Reovirus efficacy was examined in the KRAS mutant HCT116, and the isogenic KRAS WT Hke3 cell line, and in the non-malignant rat intestinal epithelial cell line. Apoptosis was determined by flow cytometry and TUNEL staining. Combination treatment with reovirus and irintoecan was investigated in 15 CRC cell lines, including the HCT116 p21 isogenic cell lines. Reovirus preferentially induced apoptosis in KRAS mutant HCT116 cells compared to its isogenic KRAS WT derivative, and in KRAS mutant IEC cells. Reovirus showed a greater degree of caspase 3 activation with PARP 1 cleavage, and preferential inhibition of p21 protein expression in KRAS mutant cells. Reovirus synergistically induced growth inhibition when combined with irinotecan. This synergy was lost upon p21 gene knock out. Reovirus preferentially induces apoptosis in KRAS mutant colon cancer cells. Reovirus and irinotecan combination therapy is synergistic, p21 mediated, and represents a novel potential treatment for patients with CRC.

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“…While it has been well established that IFN is dispensable for reovirus-induced apoptosis (40,75), we propose a model whereby IFN-mediated cytoplasmic Daxx expression lowers the apoptotic threshold by promoting death receptor signaling. However, our studies also demonstrated that Daxx has additional roles in the context of apoptosis, including inhibition of the expression of caspase 3 (Fig.…”

Section: Discussionmentioning

confidence: 85%

Daxx Upregulation within the Cytoplasm of Reovirus-Infected Cells Is Mediated by Interferon and Contributes to Apoptosis

Dionne

Zhuang

Leser

et al. 2013

J Virol

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f Reovirus infection is a well-characterized experimental system for the study of viral pathogenesis and antiviral immunity within the central nervous system (CNS). We have previously shown that c-Jun N-terminal kinase (JNK) and the Fas death receptor each play a role in neuronal apoptosis occurring in reovirus-infected brains. Death-associated protein 6 (Daxx) is a cellular protein that mechanistically links Fas signaling to JNK signaling in several models of apoptosis. In the present study, we demonstrate that Daxx is upregulated in reovirus-infected brain tissue through a type I interferon-mediated mechanism. Daxx upregulation is limited to brain regions that undergo reovirus-induced apoptosis and occurs in the cytoplasm and nucleus of neurons. Cytoplasmic Daxx is present in Fas-expressing cells during reovirus encephalitis, suggesting a role for Daxx in Fas-mediated apoptosis following reovirus infection. Further, in vitro expression of a dominant negative form of Daxx (DN-Daxx), which binds to Fas but which does not transmit downstream signaling, inhibits apoptosis of reovirus-infected cells. In contrast, in vitro depletion of Daxx results in increased expression of caspase 3 and apoptosis, suggesting that Daxx plays an antiapoptotic role in the nucleus. Overall, these data imply a regulatory role for Daxx in reovirus-induced apoptosis, depending on its location in the nucleus or cytoplasm.

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Apoptosis Induced by Mammalian Reovirus Is Beta Interferon (IFN) Independent and Enhanced by IFN Regulatory Factor 3- and NF-κB-Dependent Expression of Noxa

Cited by 46 publications

References 91 publications

Expression pattern and transcriptional regulatory mechanism of noxa gene in grass carp (Ctenopharyngodon idella)

Expression pattern and transcriptional regulatory mechanism of noxa gene in grass carp (Ctenopharyngodon idella)

Oncolytic reovirus preferentially induces apoptosis in KRAS mutant colorectal cancer cells, and synergizes with irinotecan

Daxx Upregulation within the Cytoplasm of Reovirus-Infected Cells Is Mediated by Interferon and Contributes to Apoptosis

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