2021
DOI: 10.1016/j.rvsc.2021.07.028
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Evaluation of the oncolytic property of recombinant Newcastle disease virus strain R2B in 4T1 and B16-F10 cells in-vitro

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Cited by 5 publications
(5 citation statements)
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“…In our study, we observed a significant loss of MMP, time-dependent degradation of Bcl-2 protein, time-dependent increase in Bid cleavage, mitochondrial translocation of Bax, and release of mitochondrial Cyt C following NDV infection. These findings are consistent with previous studies [26,67,68] and clearly demonstrate that NDV infection induces mitochondrial dysfunction, ultimately resulting in mitochondria-dependent apoptosis. Importantly, we discovered that inhibiting either CTSB or CTSD activity effectively mitigates NDVinduced mitochondria-dependent apoptosis, providing further support for the role of LMPinduced translocated cathepsins in mitochondrial dysfunction and subsequent activation of cell apoptosis.…”
Section: Plos Pathogenssupporting
confidence: 93%
“…In our study, we observed a significant loss of MMP, time-dependent degradation of Bcl-2 protein, time-dependent increase in Bid cleavage, mitochondrial translocation of Bax, and release of mitochondrial Cyt C following NDV infection. These findings are consistent with previous studies [26,67,68] and clearly demonstrate that NDV infection induces mitochondrial dysfunction, ultimately resulting in mitochondria-dependent apoptosis. Importantly, we discovered that inhibiting either CTSB or CTSD activity effectively mitigates NDVinduced mitochondria-dependent apoptosis, providing further support for the role of LMPinduced translocated cathepsins in mitochondrial dysfunction and subsequent activation of cell apoptosis.…”
Section: Plos Pathogenssupporting
confidence: 93%
“…A classic antitumor mechanism employed by OVs is replication within cancer cells, followed by direct lysis of these cells; this mechanism is termed direct virus-induced oncolysis (Figure 2) [40]. Consequently, transgenes are expressed and trigger host immune responses, thereby activating antitumor immunity [69] It has been reported that an engineered Newcastle disease virus leads to the loss of mitochondrial membrane permeability in tumor cells, followed by ICD [70]. The M1 virus induces endoplasmic reticulum stress-mediated apoptosis, followed by cytolysis of tumor cells [71].…”
Section: Direct Tumor Lysismentioning
confidence: 99%
“…This mechanism induces tumor cell death locally by direct tumor lysis, but it also triggers a systemic response by activating the immune system (Figure 2D) and activates the endothelial cells involved in the vascularization of the tumor, reducing tumor angiogenesis [73]. It has been reported that an engineered Newcastle disease virus leads to the loss of mitochondrial membrane permeability in tumor cells, followed by ICD [70]. The M1 virus induces endoplasmic reticulum stress-mediated apoptosis, followed by cytolysis of tumor cells [71].…”
Section: Direct Tumor Lysismentioning
confidence: 99%
“…When an oncolytic virus infects and replicates in tumor cells, it affects the synthesis of nucleic acid and protein in cells and damages organelles such as lysosomes, endoplasmic reticulum, and mitochondria, leading to alterations in cell function and, finally, killing tumor cells (Figure 1). For example, the recombinant Newcastle disease virus R2B-GFP virus causes the loss of mitochondrial membrane permeability in 4T1 and B16-F10 cells, resulting in cell death (Ramamurthy et al, 2021). The M1 virus kills cancer cells by inducing endoplasmic reticulum stress-mediated apoptosis (Lin et al, 2014).…”
Section: Direct Oncolysismentioning
confidence: 99%