2020
DOI: 10.1172/jci129497
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HPV16 drives cancer immune escape via NLRX1-mediated degradation of STING

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Cited by 117 publications
(138 citation statements)
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“…Many pre-existing scientific researches have demonstrated that the occurrence and progression of tumors are strongly related to immune cells and chemokines in the human body (Han et al, 2019;Rosenthal et al, 2019), which can be verified through the mechanism of immune escape (Luo et al, 2019). In some diseases and tumor biological processes, the changes of these immune biomarkers are clear and even can be predicted in the immune microenvironment (Silva-Santos et al, 2019).…”
Section: Discussionmentioning
confidence: 98%
“…Many pre-existing scientific researches have demonstrated that the occurrence and progression of tumors are strongly related to immune cells and chemokines in the human body (Han et al, 2019;Rosenthal et al, 2019), which can be verified through the mechanism of immune escape (Luo et al, 2019). In some diseases and tumor biological processes, the changes of these immune biomarkers are clear and even can be predicted in the immune microenvironment (Silva-Santos et al, 2019).…”
Section: Discussionmentioning
confidence: 98%
“…E7 from the high-risk mucosal HPVs represses IRF1 activity, leading to decreased IFN-β gene expression [21,36,37]. Both high-risk mucosal HPV16 and HPV18 antagonize the adaptor protein within the dsDNA signaling pathway Stimulator of IFN genes (STING) to repress signaling through the cytosolic DNA receptor pathway, although they do this through different mechanisms [20,38]. Further, HPV18 E7 can epigenetically silence RIGI, the DNA sensor cyclic GMP-AMP synthase (cGAS), and STING preventing upregulation of IFN and IFN-stimulated genes activated by dsRNA and dsDNA [39].…”
Section: Discussionmentioning
confidence: 99%
“…Many studies have reported the role of metabolism, RNA degradation and RNA transport in OSCC [34][35][36]. Human papillomavirus (HPV) is closely associated with OSCC [37]. HPV infection signi cantly increases the number of binding sites for RBPs and subsequently upregulates a group of oncogenic genes by absorbing RBPs [38].…”
Section: Discussionmentioning
confidence: 99%