Proteome Analysis in a Mammalian Cell Line Reveals that PLK2 Is Involved in Avian Metapneumovirus Type C (aMPV/C)-Induced Apoptosis

Quan, Rong; Wei, Li; Hou, Lei; Wang, Jing; Zhu, Shanshan; Li, Zixuan; Lv, Moran; Liu, Jue

doi:10.3390/v12040375

Cited by 6 publications

(7 citation statements)

References 61 publications

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“…Numerous studies have shown that viruses replicate in host cells by utilizing the host signal pathways and/or proteins. A recent report of iTRAQ quantitative proteomics showed that multiple signaling pathways, such as mTOR, MAPK, and p53, participate in aMPV/C replication [ 9 ]. In this study, a series of experiments were carried out to determine the influence of NCL on viral replication.…”

Section: Discussionmentioning

confidence: 99%

“…This is the first report of aMPV/C infection in chicken. It has been reported that aMPV/C participated in the regulation of multiple biological processes for viral replication [8,9]. Nucleolin (NCL), a highly conserved protein during evolution that is located in the nucleolus [10][11][12], participates in a variety of biological processes, such as chromatin organization and stability, ribosome biogenesis, apoptosis regulation, and stress response [13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

“…Based on genetic characterization and antigenic features, aMPV can be classified into four subgroups: A, B, C, and D [ 6 ]. Subgroup C aMPV (aMPV/C) was first successfully isolated from turkeys in the United States, and subsequently, aMPV/C was successfully isolated from farm ducks, pheasants, and wild birds in France and South Korea [ 7 , 8 , 9 ]. We isolated aMPV/C from infected meat-type chickens with severe respiratory symptoms in southern China [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

“…This is the first report of aMPV/C infection in chicken. It has been reported that aMPV/C participated in the regulation of multiple biological processes for viral replication [ 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

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Interaction of Nucleolin with the Fusion Protein of Avian Metapneumovirus Subgroup C Contributes to Viral Replication

Wang

Hou

Zhu

et al. 2022

Viruses

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Avian metapneumovirus subgroup C (aMPV/C) is highly pathogenic to various avian species with acute respiratory tract clinicopathology and/or drops in egg production. Nucleolin (NCL), an important nucleolar protein, has been shown to regulate multiple viral replication and serve as a functional receptor for viral entry and internalization. Whether NCL is involved in aMPV/C pathogenesis is not known. In this study, we found that aMPV/C infection altered the subcellular localization of NCL in cultured cells. siRNA-targeted NCL resulted in a remarkable decline in aMPV/C replication in Vero cells. DF-1 cells showed a similar response after CRISPR/Cas9-mediated knock out of NCL during aMPV/C infection. Conversely, NCL overexpression significantly increased aMPV/C replication. Pretreatment with AS1411-a aptamer, a guanine (G)-rich oligonucleotide that forms four-stranded structures and competitively binding to NCL, decreased aMPV/C replication and viral titers in cultured cells. Additionally, we found that the aMPV/C fusion (F) protein specifically interacts with NCL through its central domain and that AS1411 disrupts this interaction, thus inhibiting viral replication. Taken together, these results reveal that the aMPV/C F protein interacts with NCL, which is employed by aMPV/C for efficient replication, thereby highlighting the strategic potential for control and therapy of aMPV/C infection.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…This is the first report of aMPV/C infection in chicken. It has been reported that aMPV/C participated in the regulation of multiple biological processes for viral replication [ 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Interaction of Nucleolin with the Fusion Protein of Avian Metapneumovirus Subgroup C Contributes to Viral Replication

Wang

Hou

Zhu

et al. 2022

Viruses

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“…Besides, avian metapneumovirus subtype C (aMPV/C) infection leads to upregulation of PLK2 in mammalian cells. Inhibition of PLK2 could reduce ROS production and p53-dependant apoptosis induced by aMPV/C, and decrease the virus release, suggesting that the high expression of PLK2 is associated with aMPV/C-induced apoptosis and viral replication ( 89 ). Contrasting to its family members, PLK2 is poorly studied in viral infection, and the exact role and mechanism remain unclear.…”

Section: Role Of Plk2 In Basic Pathophysiological Processesmentioning

confidence: 99%

Polo-Like Kinase 2: From Principle to Practice

Zhang

2022

Front. Oncol.

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Polo-like kinase (PLK) 2 is an evolutionarily conserved serine/threonine kinase that shares the n-terminal kinase catalytic domain and the C-terminal Polo Box Domain (PBD) with other members of the PLKs family. In the last two decades, mounting studies have focused on this and tried to clarify its role in many aspects. PLK2 is essential for mitotic centriole replication and meiotic chromatin pairing, synapsis, and crossing-over in the cell cycle; Loss of PLK2 function results in cell cycle disorders and developmental retardation. PLK2 is also involved in regulating cell differentiation and maintaining neural homeostasis. In the process of various stimuli-induced stress, including oxidative and endoplasmic reticulum, PLK2 may promote survival or apoptosis depending on the intensity of stimulation and the degree of cell damage. However, the role of PLK2 in immunity to viral infection has been studied far less than that of other family members. Because PLK2 is extensively and deeply involved in normal physiological functions and pathophysiological mechanisms of cells, its role in diseases is increasingly being paid attention to. The effect of PLK2 in inhibiting hematological tumors and fibrotic diseases, as well as participating in neurodegenerative diseases, has been gradually recognized. However, the research results in solid organ tumors show contradictory results. In addition, preliminary studies using PLK2 as a disease predictor and therapeutic target have yielded some exciting and promising results. More research will help people better understand PLK2 from principle to practice.

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Inhibition of Polo-like kinase 1 (PLK1) triggers cell apoptosis via ROS-caused mitochondrial dysfunction in colorectal carcinoma

Feng

Lin

et al. 2023

J Cancer Res Clin Oncol

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Colorectal cancer (CRC) is one of the most frequently diagnosed cancers. Polo-like kinase 1 (PLK1), a member of the serine/threonine kinase PLK family, is the most investigated and essential in the regulation of cell cycle progression, including chromosome segregation, centrosome maturation and cytokinesis. However, the nonmitotic role of PLK1 in CRC is poorly understood. In this study, we explored the tumorigenic effects of PLK1 and its potential as a therapeutic target in CRC. First, immunohistochemistry analysis revealed the signi cant accumulation of PLK1 in patient-derived CRC tissues compared with adjacent healthy tissues. Furthermore, PLK1 inhibition genetically or pharmacologically signi cantly reduced cell viability, migration and colony formation, and triggered apoptosis of CRC cells. Additionally, we found that PLK1 inhibition elevated cellular reactive oxygen species (ROS) accumulation and decreased the Bcl2/Bax ratio, which led to mitochondrial dysfunction and the release of Cytochrome c, a key process in initiating cell apoptosis. In summary, these data provide new insights into the pathogenesis of CRC and support the potential value of PLK1 as an appealing target for CRC treatment. Overall, the underlying mechanism of inhibiting PLK1-induced apoptosis indicates that the PLK1 inhibitor BI6727 may be a novel potential therapeutic strategy in the treatment of CRC.

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Proteome Analysis in a Mammalian Cell Line Reveals that PLK2 Is Involved in Avian Metapneumovirus Type C (aMPV/C)-Induced Apoptosis

Cited by 6 publications

References 61 publications

Interaction of Nucleolin with the Fusion Protein of Avian Metapneumovirus Subgroup C Contributes to Viral Replication

Interaction of Nucleolin with the Fusion Protein of Avian Metapneumovirus Subgroup C Contributes to Viral Replication

Polo-Like Kinase 2: From Principle to Practice

Inhibition of Polo-like kinase 1 (PLK1) triggers cell apoptosis via ROS-caused mitochondrial dysfunction in colorectal carcinoma

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