HN Protein of Newcastle Disease Virus Induces Apoptosis Through SAPK/JNK Pathway

Rajmani, R. S.; Gandham, Ravi Kumar; Gupta, Shishir Kumar; Sahoo, Aditya Prasad; Singh, Prafull; Kumar, Rajiv; Saxena, Shikha; Chaturvedi, Uttara; Tiwari, Ashok Kumar

doi:10.1007/s12010-015-1788-7

Cited by 16 publications

(16 citation statements)

References 47 publications

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“…We have demonstrated the activation of the SAPK/JNK pathway by HN [13]. HeLa cells are naturally resistant to TNF-a-induced cytotoxicity but may become sensitized when NF-jB transactivation is blocked or cells are treated with compounds that inhibit protein synthesis [20].…”

Section: Discussionmentioning

confidence: 94%

“…This assay was performed using a method reported in our previous studies [9,13]. Briefly, harvested cells (48 h post-transfection [p.t.])…”

Section: Dna Fragmentation Assaymentioning

confidence: 99%

“…The assay was performed as described previously [13]. Briefly, cells at 48 h p.t were harvested, washed with PBS and fixed using 70 % ice-cold ethanol and stored at -20°C overnight.…”

Section: Propidium Iodide Stainingmentioning

confidence: 99%

“…We further speculated that NF-jB downregulation might also sensitize the cells to TNF-a-mediated apoptosis [13]. Recently, cytokines with anti-tumor properties have gained importance in cancer gene therapy [17].…”

Section: Introductionmentioning

confidence: 99%

“…Newcastle disease virus (NDV) has inherent oncolytic properties because its multifunctional protein HN specifically activates the apoptotic machinery of tumor cells by upregulating the expression of ''TNF-related apoptosis-inducing ligand'' (TRAIL) and interferon-a [11][12][13]. HN protein has been shown to induce apoptosis in chicken embryo fibroblast (CEF) cells [14], human hepatoma SMMC-7721 cells [11], and MCF-7 cells [15].…”

Section: Introductionmentioning

confidence: 99%

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HN protein of Newcastle disease virus sensitizes HeLa cells to TNF-α-induced apoptosis by downregulating NF-κB expression

et al. 2016

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Newcastle disease virus (NDV) is an oncolytic virus which selectively replicates in tumor cells and exerts anti-tumor cytotoxic activity by promoting cell death. In this study, we focus on characterization of the underlying mechanisms of NDV-induced cell death in HeLa cells. We find that NDV Herts/33 strain triggers both extrinsic and intrinsic apoptosis at late infection times. The activation of NF-кB pathway and subsequent up-regulation of TNF-α/TRAIL initiates extrinsic apoptosis, leading to activation of caspase 8 and cleavage of Bid into tBid. tBid transmits the extrinsic apoptotic signals to mitochondria and mediates intrinsic apoptosis, which is hallmarked by cleavage of caspase 9. Moreover, RIP1 is cleaved into RIP1-N and RIP1-C at D324 by caspase 8, and this cleavage promotes apoptosis. Surprisingly, over expression of RIP1 reduces apoptosis and depletion of RIP1 promotes apoptosis, suggesting full length RIP1 is anti-apoptotic. Moreover, necroptosis hallmark protein MLKL is activated by phosphorylation at 12-24 h.p.i., and RIP1 regulates the level of phosphor-MLKL. Immunostaining shows that RIP1 aggregates to stress granules (SGs) at 8-24 h.p.i., and phosphor-MLKL is also recruited to SGs, instead of migrating to plasma membrane to exert its necrotic function. Immunoprecipitation study demonstrates that RIP1 bind to phosphor-MLKL, and depletion of RIP1 reduces the aggregation of MLKL to SGs, suggesting that RIP1 recruits MLKL to SGs. Altogether, NDV infection initiates extrinsic apoptosis via activation of NF-кB and secretion of TNF-α/TRAIL. Activation of caspase 8 by TNF-α/TRAIL and subsequent cleavage of Bid and RIP1 transmit the death signals to mitochondria. Meanwhile, virus subverts the host defensive necroptosis via recruiting phosphor-MLKL by RIP1 to SGs. Thus, RIP1 is a central signaling protein in regulation of apoptosis and necroptosis during NDV infection. www.impactjournals.com/oncotarget/

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Section: Discussionmentioning

confidence: 94%

“…This assay was performed using a method reported in our previous studies [9,13]. Briefly, harvested cells (48 h post-transfection [p.t.])…”

Section: Dna Fragmentation Assaymentioning

confidence: 99%

“…The assay was performed as described previously [13]. Briefly, cells at 48 h p.t were harvested, washed with PBS and fixed using 70 % ice-cold ethanol and stored at -20°C overnight.…”

Section: Propidium Iodide Stainingmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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HN protein of Newcastle disease virus sensitizes HeLa cells to TNF-α-induced apoptosis by downregulating NF-κB expression

et al. 2016

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Identification of long noncoding RNAs of silkworm at the early stage of Bombyx mori bidensovirus infection

Chen,

Wang,

et al. 2024

Arch Insect Biochem Physiol

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Bombyx mori bidensovirus (BmBDV) is one of the most important pathogens of silkworm. It mainly infects midgut cells of silkworm and causes losses to the sericulture industry. Long noncoding RNAs (lncRNAs) have been reported to play an important role in the regulation of antiviral immune response in silkworm. To explore whether lncRNAs are involved in BmBDV infection and immune response of silkworm, we performed a comparative transcriptome analysis to identify the lncRNAs and mRNAs between the BmBDV infected and noninfected silkworm larvae at the early stage. A total of 16,069 genes and 974 candidate lncRNAs were identified, among which 142 messenger RNA (mRNAs) and four lncRNAs were differentially expressed (DE). Target gene prediction revealed that 142 DEmRNAs were coexpressed with four DElncRNAs, suggesting that the expression of mRNA is mainly affected through trans‐regulation activities. A regulatory network of DElncRNAs and DEmRNAs was constructed, showing that many genes targeted by different DElncRNAs are involved in metabolism and immunity, which implies that these genes and lncRNAs play an important role in the replication of BmBDV. Our results will help us to improve our understanding of lncRNA‐mediated regulatory roles in BmBDV infection, providing a new perspective for further exploring the interaction between host and BmBDV.

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The Role of ΔFosB on the Pro-survival Effect of PTHrP in Goat Mammary Epithelial Cells

Yao

Zheng

2016

Appl Biochem Biotechnol

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The mechanism of regulation mammary epithelial cell number in ruminant is not fully understood, but is thought to be dependent on the balance of cell proliferation and cell apoptosis. Parathyroid hormone-related protein (PTHrP) could express in mammary epithelial cells and breast cancer cells, and has been reported to regulate cell survival. Here, we showed that PTHrP induced cell proliferation and increased the expression of CyclinD1 and proliferating cell nuclear antigen (PCNA) in goat mammary epithelial cells (GMEC). PTHrP increased the mRNA levels of anti-apoptosis genes Bcl-2 and Bcl-xl, and protected GMEC from apoptosis. We also found ΔFosB, an alternative splicing of finkel-biskis-jinkins murine osteosarcoma B (fosB), inhibited GMEC apoptosis, and induced cell proliferation with increased Bcl-2/Bax and Bcl-xl/Bax ratios. Interestingly, ΔFosB could further promote the pro-survival effect of PTHrP, and the Bcl-2/Bax and Bcl-xl/Bax ratios showed higher levels. We conclude that the pro-survival role of PTHrP in GMEC may be regulated by ΔFosB.

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HN Protein of Newcastle Disease Virus Induces Apoptosis Through SAPK/JNK Pathway

Cited by 16 publications

References 47 publications

HN protein of Newcastle disease virus sensitizes HeLa cells to TNF-α-induced apoptosis by downregulating NF-κB expression

HN protein of Newcastle disease virus sensitizes HeLa cells to TNF-α-induced apoptosis by downregulating NF-κB expression

Identification of long noncoding RNAs of silkworm at the early stage of Bombyx mori bidensovirus infection

The Role of ΔFosB on the Pro-survival Effect of PTHrP in Goat Mammary Epithelial Cells

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