Inhibitory and Apoptosis-Inducing Effects of Newcastle Disease Virus Strain AF2240 on Mammary Carcinoma Cell Line

Ahmad, Umar; Ahmed, Ismaila; Yong, Yoke Keong; Manan, Nizar Abd; Othman, Fauziah

doi:10.1155/2015/127828

Cited by 25 publications

(26 citation statements)

References 38 publications

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“…NDV is known to cause inhibition of migration in various types of cancer cells 26,27 . However, the underlying mechanism is not well known.…”

Section: Discussionmentioning

confidence: 99%

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Newcastle disease virus mediated apoptosis and migration inhibition of human oral cancer cells: A probable role of β-catenin and matrix metalloproteinase-7

Morla

Kumar

2019

Sci Rep

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Cancer cell metastasis and its dissemination are most enigmatic and challenging aspects in the development of its therapeutics. Newcastle disease virus (NDV) is a well-studied avian paramyxovirus frequently isolated from birds and rarely from mammals. Since the first report of its oncolytic property, many NDV strains were studied for its effect in various cancer cells. In the present study, NDV strain Bareilly was characterized for its apoptotic potential and migration inhibition in human oral cancer cells. The NDV mediated apoptosis was confirmed by flow cytometry, DNA laddering, and immunoblotting. Moreover, NDV decreased the mitochondrial membrane potential suggesting an intrinsic pathway of apoptosis in oral cancer cells. NDV infection in oral cancer cells results in migration inhibition by a reduction in levels of MMP-7. MMP-7 is one of the key target genes of β-catenin. While overexpression of MMP-7 reversed the inhibitory effect of NDV mediated migration suggested its possible involvement. Wnt/β-catenin is an essential pathway for cell growth, differentiation, and metastasis. The involvement of the Wnt/β-catenin pathway in NDV infection has never been reported. Our results showed that NDV dysregulates Wnt/β-catenin by down-regulation of p-Akt and p-GSK3β leading to degradation of β-catenin. Furthermore, NDV infection leads to a reduction in cytoplasmic and nuclear levels of β-catenin. The study will provide us with a better insight into the molecular mechanism of NDV mediated oncolysis and the key cellular partners involved in the process.

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“…NDV is known to cause inhibition of migration in various types of cancer cells 26,27 . However, the underlying mechanism is not well known.…”

Section: Discussionmentioning

confidence: 99%

“…MMP-1, -2, -7, -9 and -14 are well studied and known to be elevated in various cancer cells 24,25 . NDV mediated inhibition of cancer cell migration was reported in various cancer cells 26,27 . Although the studies are confined to MMP-2 and -9, its underlying molecular mechanism is not addressed.…”

Section: Introductionmentioning

confidence: 99%

Newcastle disease virus mediated apoptosis and migration inhibition of human oral cancer cells: A probable role of β-catenin and matrix metalloproteinase-7

Morla

Kumar

2019

Sci Rep

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“…On the other hand, a number of viruses may enhance host cell viability to prolong the release of virus particles ( 10 , 15 ). Recent studies revealed that apoptosis was induced in cultured and primary cells by some members of the family Paramyxiviridae such as Newcastle disease virus ( 16 , 17 ), Sendai virus ( 18 , 19 ), canine distemper virus ( 20 , 21 ), and peste des petits ruminants virus ( 22 ). The apoptotic mechanisms of these viruses were further evaluated.…”

Section: Introductionmentioning

confidence: 99%

Bta-miR-98 Suppresses Replication of Caprine Parainfluenza Virus Type 3 Through Inhibiting Apoptosis by Targeting Caspase-3

Zhong

Liao

et al. 2020

Front. Immunol.

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Caprine parainfluenza virus type 3 (CPIV3) is an emerging respiratory pathogen that affects the sheep and goat industry in China and possibly other countries around the world. Accumulating evidence suggests that microRNAs play important roles in regulating virus-host interactions and can suppress or facilitate viral replication. In this study, we showed that CPIV3 infection induced apoptosis in Madin-Darby bovine kidney (MDBK) cells, as determined by morphological changes and flow cytometry. Caspase activity and the expression of pro-apoptotic genes further indicated that CPIV3 induced apoptosis by activating both the intrinsic and extrinsic pathways. We also demonstrated the involvement of bta-microRNA-98 (bta-miR-98) in regulating CPIV3-induced apoptosis. Bta-miR-98 was downregulated in MDBK cells infected with CPIV3. Overexpression of bta-miR-98 significantly decreased the activities of caspase-3, −8, and −9. Conversely, inhibition of bta-miR-98 had completely opposite effects. Furthermore, our data showed that bta-miR-98 markedly affected CPIV3 replication by regulating apoptosis. Importantly, we found that bta-miR-98 modulated CPIV3-induced apoptosis by targeting caspase-3, an effector of apoptosis. Collectively, our results may suggest that CPIV3 infection induced apoptosis and downregulated the levels of bta-miR-98, and this miRNA regulated viral replication through effected apoptosis. This study contributes to our understanding of the molecular mechanisms underlying CPIV3 pathogenesis.

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“…The suppression of migration observed in this set-up was a direct effect of the reduction in cell proliferation due to apoptosis induction (Ahmad et al, 2015). …”

Section: Cell Death In Response To Ndv Infectionmentioning

confidence: 91%

The therapeutic effect of death: Newcastle disease virus and its antitumor potential

et al. 2015

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Programmed cell death is essential to survival of multicellular organisms. Previously restricted to apoptosis, the concept of programmed cell death is now extended to other mechanisms, as programmed necrosis or necroptosis, autophagic cell death, pyroptosis and parthanatos, among others. Viruses have evolved to manipulate and take control over the programmed cell death response, and the infected cell attempts to neutralize viral infections displaying different stress signals and defensive pathways before taking the critical decision of self-destruction. Learning from viruses and their interplay with the host may help us to better understand the complexity of the self-defense death response that when altered might cause disorders as important as cancer. In addition, as the fields of immunotherapy and oncolytic viruses advance as promising novel cancer therapies, the programmed cell death response reemerges as a key point for the success of both therapeutic approaches. In this review we summarize the research of the multimodal cell death response induced by Newcastle disease viruses (NDV), considered nowadays a promising viral oncolytic therapeutic, and how the manipulation of the host programmed cell death response can enhance the NDV antitumor capacity.

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Inhibitory and Apoptosis-Inducing Effects of Newcastle Disease Virus Strain AF2240 on Mammary Carcinoma Cell Line

Cited by 25 publications

References 38 publications

Newcastle disease virus mediated apoptosis and migration inhibition of human oral cancer cells: A probable role of β-catenin and matrix metalloproteinase-7

Newcastle disease virus mediated apoptosis and migration inhibition of human oral cancer cells: A probable role of β-catenin and matrix metalloproteinase-7

Bta-miR-98 Suppresses Replication of Caprine Parainfluenza Virus Type 3 Through Inhibiting Apoptosis by Targeting Caspase-3

The therapeutic effect of death: Newcastle disease virus and its antitumor potential

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