Signal Transducer and Activator of Transcription 3 Signaling in Tumor Immune Evasion

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dc.contributor.authorZhang, Luyingcs
dc.contributor.authorKuča, Kamilcs
dc.contributor.authorYou, Lics
dc.contributor.authorZhao, Yingyingcs
dc.contributor.authorMusílek, Kamilcs
dc.contributor.authorNepovimová, Eugeniecs
dc.contributor.authorWu, Qinghuacs
dc.contributor.authorWu, Wendacs
dc.contributor.authorAdam, Vojtěchcs
dc.coverage.issue1cs
dc.coverage.volume230cs
dc.date.accessioned2022-09-16T14:50:29Z
dc.date.available2022-09-16T14:50:29Z
dc.date.issued2022-02-28cs
dc.description.abstractThe underlying mechanism of tumor immune evasion is a highly concerning subject for researchers. Increasing evidences reveal that the over-activated signal transducer and activator of transcription 3 (STAT3) is a crucial molecular hub in malignant tumors. STAT3 controls autophagy molecules that impair CTL-mediated tumor cell lysis, inhibiting natural killer cells and inducing apoptosis in T lymphocytes to create an immunosuppressive environment. STAT3 signaling regulates the expression of immune factors and recruits immunosuppressive cells to establish a tolerant tumor microenvironment (TME). STAT3 signaling regulates the expression of immune factors and recruits immunosuppressive cells to create an immunosuppressive environment. All this aid tumor cells in escaping from immune surveillance. In this review, we outlined the STAT3-mediated mechanisms involved in tumor immune evasion and their potential regulatory functions in the TME. We discussed the impact of STAT3 signaling on PD-L1, HIF-1, exosome, lncRNA, and autophagy in the promotion of tumor immune evasion and highlighted the recent research on STAT3 signaling and tumor immune evasion that may assist in developing effective STAT3-targeted drugs for advancing immunotherapy.en
dc.description.embargo2024-03-04cs
dc.formattextcs
dc.format.extent1-11cs
dc.format.mimetypeapplication/pdfcs
dc.identifier.citationPHARMACOLOGY & THERAPEUTICS. 2022, vol. 230, issue 1, p. 1-11.en
dc.identifier.doi10.1016/j.pharmthera.2021.107969cs
dc.identifier.issn0163-7258cs
dc.identifier.other177313cs
dc.identifier.urihttp://hdl.handle.net/11012/208402
dc.language.isoencs
dc.publisherElseviercs
dc.relation"European Union (EU)" & "Horizon 2020"en
dc.relation.ispartofPHARMACOLOGY & THERAPEUTICScs
dc.relation.urihttps://www.sciencedirect.com/science/article/pii/S0163725821001716cs
dc.rightsCreative Commons Attribution-NonCommercial-NoDerivatives 4.0 Internationalcs
dc.rights.accessopenAccesscs
dc.rights.sherpahttp://www.sherpa.ac.uk/romeo/issn/0163-7258/cs
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/cs
dc.subjectImmune evasionen
dc.subjectlncRNAen
dc.subjectSTAT3en
dc.subjectTumor microenvironmenten
dc.titleSignal Transducer and Activator of Transcription 3 Signaling in Tumor Immune Evasionen
dc.type.driverarticleen
dc.type.statusPeer-revieweden
dc.type.versionacceptedVersionen
sync.item.dbidVAV-177313en
sync.item.dbtypeVAVen
sync.item.insts2023.03.27 12:52:56en
sync.item.modts2023.03.27 12:14:24en
thesis.grantorVysoké učení technické v Brně. Středoevropský technologický institut VUT. Chytré nanonástrojecs
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