Aberrant PD-1 ligand expression contributes to the myocardial inflammatory injury caused by Coxsackievirus B infection

Wang, Tianying; Chen, Shuang; Wang, Xueqing Wang; Huang, Yike; Qiu, Jianfa; Fei, Yanru; Chaulagain, Anita; Yang, Chen; Lin, Lexun; Yan, Bin; Wang, Ying; Wang, Wei; Zhao, Wenran; Zhong, Zhaohua

doi:10.1016/j.antiviral.2019.03.007

Cited by 7 publications

(5 citation statements)

References 59 publications

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“…Although these changes in PD-L1 mRNA levels can be imputed to gene transcription regulation, many studies have demonstrated that PD-L1 could be regulated at the posttranscriptional level. After treatment with actinomycin D, the half-life of PD-L1 mRNA was about 3 h in MDA-MB-231 [110] and HeLa cells [111]. In these two studies, TTP (tristetraprolin) and AUF1 (AU-rich element-binding protein 1) bounded to 3 -UTR and modulated mRNA stability.…”

Section: Posttranscriptional and Posttranslational Regulationsmentioning

confidence: 84%

The Role of Oncogenes and Redox Signaling in the Regulation of PD-L1 in Cancer

Glorieux

Xia

Huang

2021

Cancers

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Tumor cells can evade the immune system via multiple mechanisms, including the dysregulation of the immune checkpoint signaling. These signaling molecules are important factors that can either stimulate or inhibit tumor immune response. Under normal physiological conditions, the interaction between programmed cell death ligand 1 (PD-L1) and its receptor, programmed cell death 1 (PD-1), negatively regulates T cell function. In cancer cells, high expression of PD-L1 plays a key role in cancer evasion of the immune surveillance and seems to be correlated with clinical response to immunotherapy. As such, it is important to understand various mechanisms by which PD-L1 is regulated. In this review article, we provide an up-to-date review of the different mechanisms that regulate PD-L1 expression in cancer. We will focus on the roles of oncogenic signals (c-Myc, EML4-ALK, K-ras and p53 mutants), growth factor receptors (EGFR and FGFR), and redox signaling in the regulation of PD-L1 expression and discuss their clinical relevance and therapeutic implications. These oncogenic signalings have common and distinct regulatory mechanisms and can also cooperatively control tumor PD-L1 expression. Finally, strategies to target PD-L1 expression in tumor microenvironment including combination therapies will be also discussed.

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Section: Posttranscriptional and Posttranslational Regulationsmentioning

confidence: 84%

The Role of Oncogenes and Redox Signaling in the Regulation of PD-L1 in Cancer

Glorieux

Xia

Huang

2021

Cancers

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“…We found that the significantly downregulated proteins were involved in BPs, including multiple catabolic processes and, interestingly, some virus-related processes. As our previous research noted, during viral infection (Coxsackievirus Group B), AUF1 played a role in viral mRNA stability and the inflammatory response [ 2 , 22 ]. Therefore, the downstream target of AUF1 involved in viral infection received more attention.…”

Section: Resultsmentioning

confidence: 99%

“…Overexpression Associated with AUF1 Expression. Based on our previous data, CVB could cleave AUF1 by its 3C protease [22]. To elucidate the consequent effect of DDX5 regulation by AUF1 during CVB infection and its potential role in viral replication, we first knocked down AUF1 expression in HeLa cells with siRNA.…”

Section: Cvb Replication Was Promoted By Ddx5mentioning

confidence: 99%

Cleavage of AUF1 by Coxsackievirus B Affects DDX5 Regulatory on Viral Replication through iTRAQ Proteomics Analysis

Wang

Qin

Chen

et al. 2022

BioMed Research International

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Coxsackievirus B (CVB) 3C protease (3Cpro) plays a specific cleavage role on AU-rich binding factor (AUF1, also called hnRNP D), which consequently disputes the regulation of AUF1 on downstream molecules. In our study, the iTRAQ approach was first used to quantify the differentially expressed cellular proteins in AUF1-overexpressing HeLa cells, which provides straightforward insight into the role of AUF1 during viral infection. A total of 1,290 differentially expressed proteins (DEPs), including 882 upregulated and 408 downregulated proteins, were identified. The DEPs are involved in a variety of cellular processes via GO terms, protein–protein interactions, and a series of further bioinformatics analyses. Among the DEPs, some demonstrated important roles in cellular metabolism. In particular, DDX5 was further verified to be negatively regulated by AUF1 and increased in CVB-infected cells, which in turn promoted CVB replication. These findings provide potential novel ideas for exploring new antiviral therapy targets.

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“…The molecular mechanisms underlying the embryotoxic effect of 3Cpro are currently unclear. Picornavirus 3C protease can cleave various cellular proteins including regulatory factors, which can affect a wide range of biochemical processes [1][2][3][4][5][6][7][8] . It is worth mentioning that 3C protease activity induces cell death [9][10][11][12][13][14][15][16][17][18] , and thus can be considered as the key factor of viral cytotoxicity.…”

Section: Discussionmentioning

confidence: 99%

Embryotoxic activity of 3C protease of human hepatitis A virus in developing Danio rerio embryos

Selina

Karaseva

Komissarov

et al. 2021

Sci Rep

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The 3C protease is a key factor in picornavirus-induced pathologies with a comprehensive action on cell targets. However, the effects induced by the enzyme have not been described at the organismic level. Here, the model of developing Danio rerio embryos was used to analyze possible toxic effects of the 3C protease of human hepatitis A virus (3Cpro) at the whole-body level. The transient 3Cpro expression had a notable lethal effect and induced a number of specific abnormalities in Danio rerio embryos within 24 h. These effects are due to the proteolytic activity of the enzyme. At the same time, the 3Cpro variant with reduced catalytic activity (3Cmut) increased the incidence of embryonic abnormalities; however, this effect was smaller compared to the native enzyme form. While the expression of 3Cmut increased the overall rate of abnormalities, no predominance of specific ones was observed. The data obtained point to a presence significant impact of picornavirus 3Cprotease at the whole-organism level and make contribution to the study of the infectious process caused by human hepatitis A virus.

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Aberrant PD-1 ligand expression contributes to the myocardial inflammatory injury caused by Coxsackievirus B infection

Cited by 7 publications

References 59 publications

The Role of Oncogenes and Redox Signaling in the Regulation of PD-L1 in Cancer

The Role of Oncogenes and Redox Signaling in the Regulation of PD-L1 in Cancer

Cleavage of AUF1 by Coxsackievirus B Affects DDX5 Regulatory on Viral Replication through iTRAQ Proteomics Analysis

Embryotoxic activity of 3C protease of human hepatitis A virus in developing Danio rerio embryos

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