Non-structural protein 1 of H3N2 influenza A virus induces nucleolar stress via interaction with nucleolin

Yan, Yinxia; Du, Yongming; Wang, Gefei; Li, KS

doi:10.1038/s41598-017-18087-2

Cited by 22 publications

(20 citation statements)

References 48 publications

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“…According to this, Mdm2’s cleavage induced by caspases seems to be significant for p53’s continuous activation in oridonin‐induced apoptosis and cell cycle arrest. Additionally, oridonin has been proved to be a small inhibitor of nucleolin, which participates in nucleolar stress associated with specific ribosomal proteins . Under nucleolar stress, ribosomal proteins‐Mdm2‐p53 pathway can result in p53 stabilization and activation, so it is well worthy to further explore whether oridonin reactivates p53 via regulation on nucleolin and related ribosomal proteins …”

Section: Discussionmentioning

confidence: 99%

“…Additionally, oridonin has been proved to be a small inhibitor of nucleolin, 39 which participates in nucleolar stress associated with specific ribosomal proteins. 40 Under nucleolar stress, ribosomal proteins-Mdm2-p53 pathway can result in p53 stabilization and activation, so it is well worthy to further explore whether oridonin reactivates p53 via regulation on nucleolin and related ribosomal proteins. 41 Consistent with previous studies in other cancers, oridonin induced NB cells apoptosis and cell cycle arrest by reactivating p53.…”

Section: Discussionmentioning

confidence: 99%

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Oridonin induces Mdm2‐p60 to promote p53‐mediated apoptosis and cell cycle arrest in neuroblastoma

et al. 2019

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Oridonin could induce NB (neuroblastoma) cells growth inhibition by inducing apoptosis and cell cycle arrest, and the molecular mechanisms behind the effects deserve to be further explored. Here, oridonin was confirmed to cause the reactivation of p53 (cellular tumor antigen p53) to promote the expression of a series of apoptosis‐ and cell cycle arrest‐related proteins for the biological effects. During the process, oridonin relied on the caspase activation to cleave p53‐induced Mdm2 (E3 ubiquitin‐protein ligase Mdm2) to generate Mdm2‐p60. The generation of Mdm2‐p60 stabilized p53, and resulted in p53 accumulation for p53 continuous activation. In our research, it was also found that the reactivation of p53 induced by oridonin was closely related with the generation of ROS (reactive oxygen species). Taken together, these findings explain that oridonin exerts its anticancer activity partially by targeting the Mdm2‐p53 axis in NB cells, which lay an experimental base for future research of exploring the effects and molecular mechanisms of oridonin.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Oridonin induces Mdm2‐p60 to promote p53‐mediated apoptosis and cell cycle arrest in neuroblastoma

et al. 2019

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“…Cell nucleolin is a central hub for the replication of pathogenic RNA viruses. Previous study suggests that non-structural 1 protein (NS1) of influenza A (H3N2) could induce nucleolar stress based on epigenetic alteration of rRNA gene promoter via interaction with nucleolin [37]. In A vs. C comparison, promoter methylation of LOC100511875 has been linked with maturation of 5.8S rRNA and defense response to virus.…”

Section: Discussionmentioning

confidence: 99%

Identification of DNA methylation regulated novel host genes relevant to inhibition of virus replication in porcine PK15 cell using double stranded RNA mimics and DNA methyltransferase inhibitor

et al. 2019

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A B S T R A C TDuring RNA viruses's replication, double-stranded RNA (dsRNA) is normally produced and induce host innate immune response. Most of gene activation due cytokine mediated but which are due to methylation mediated is still unknown. In the study, DNA methylome was integrated with our previous transcriptome data to investigate the differentially methylated regions and genes using MeDIP-chip technology. We found that the transcriptional expressions of 15, 37 and 18 genes were negatively related with their promoter DNA methylation levels in the cells treated by PolyI:C, Aza-CdR, as well as PolyI:C plus Aza-CdR, respectively, compared with the untreated cells. GO analysis revealed hypo-methylated genes (BNIP3L and CDK9) and a hyper-methylated gene (ZC3HAV1) involved in the host response to viral replication. Our results suggest that these novel genes targeted by DNA methylation can be potential markers relevant to virus replication and host innate immune response to set up a medical model of infectious diseases. PolyI:C treated cells (P < 0.05) [2]. Out of these DEGs, eighteen are Abbreviations: PK15, porcine kidney epithelial cell line; dsRNA, double-stranded RNA; PolyI:C, a synthetic viral-like dsRNA analogplolyinosinic: polycyticdylic acid; Aza-CdR, DNA methyltransferases inhibitor 5-aza-2′-deoxycytidine; P, PK15 cells extracellular treatment with PolyI:C; A, PK15 cells treated with Aza-CdR; P+A, PK15 cells treated with PolyI:C followed by the addition of Aza-

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“…(Fig 5C). Tick-borne encephalitis virus and host rRNA/protein shut-off Previously, a link between the inhibition of expression of 45-47S pre-rRNA and nucleolar stress was documented [31]. There are several hallmarks typical for nucleolar stress including disruption of nucleolus structure [51].…”

Section: Tbev Interferes With De Novo Production Of 45-47s Pre-rrna Tmentioning

confidence: 99%

“…Out of all the transcripts synthesised in the eukaryotic cell, ribosomal RNA is the most abundant and a key component of ribosomes. Virus-induced interference with transcription and subsequent processing of host rRNA has been described for influenza A virus [31], herpes simplex virus type I [32], human papillomavirus type 8 [33], human cytomegalovirus [34], and human immunodeficiency virus (HIV) [35]. However, this was not described for flaviviruses.…”

Section: Introductionmentioning

confidence: 99%

Tick-borne encephalitis virus inhibits rRNA synthesis and host protein production in human cells of neural origin

et al. 2019

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Tick-borne encephalitis virus (TBEV), a member of the genus Flavivirus (Flaviviridae), is a causative agent of a severe neuroinfection. Recently, several flaviviruses have been shown to interact with host protein synthesis. In order to determine whether TBEV interacts with this host process in its natural target cells, we analysed de novo protein synthesis in a human cell line derived from cerebellar medulloblastoma (DAOY HTB-186). We observed a significant decrease in the rate of host protein synthesis, including the housekeeping genes HPRT1 and GAPDH and the known interferon-stimulated gene viperin. In addition, TBEV infection resulted in a specific decrease of RNA polymerase I (POLR1) transcripts, 18S and 28S rRNAs and their precursor, 45-47S pre-rRNA, but had no effect on the POLR3 transcribed 5S rRNA levels. To our knowledge, this is the first report of flavivirus-induced decrease of specifically POLR1 rRNA transcripts accompanied by host translational shut-off.

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Non-structural protein 1 of H3N2 influenza A virus induces nucleolar stress via interaction with nucleolin

Cited by 22 publications

References 48 publications

Oridonin induces Mdm2‐p60 to promote p53‐mediated apoptosis and cell cycle arrest in neuroblastoma

Oridonin induces Mdm2‐p60 to promote p53‐mediated apoptosis and cell cycle arrest in neuroblastoma

Identification of DNA methylation regulated novel host genes relevant to inhibition of virus replication in porcine PK15 cell using double stranded RNA mimics and DNA methyltransferase inhibitor

Tick-borne encephalitis virus inhibits rRNA synthesis and host protein production in human cells of neural origin

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