Signal transducer and activator of transcription 3 signaling in tumor immune evasion
The 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 impa...
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| Published in | Pharmacology & therapeutics (Oxford) Vol. 230; p. 107969 |
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| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Elsevier Inc
01.02.2022
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| Subjects | |
| Online Access | Get full text |
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| Abstract | The 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-1α, 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. |
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| AbstractList | The 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-1α, 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. The 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-1α, 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.The 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-1α, 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. |
| ArticleNumber | 107969 |
| Author | Musilek, Kamil Wu, Qinghua Zhao, Yingying Nepovimova, Eugenie Adam, Vojtech You, Li Wu, Wenda Kuca, Kamil Zhang, Luying |
| Author_xml | – sequence: 1 givenname: Luying surname: Zhang fullname: Zhang, Luying organization: College of Life Science, Yangtze University, Jingzhou 434025, China – sequence: 2 givenname: Kamil surname: Kuca fullname: Kuca, Kamil organization: Department of Chemistry, Faculty of Science, University of Hradec Kralove, Hradec Králové 500 03, Czech Republic – sequence: 3 givenname: Li surname: You fullname: You, Li organization: College of Life Science, Yangtze University, Jingzhou 434025, China – sequence: 4 givenname: Yingying surname: Zhao fullname: Zhao, Yingying organization: College of Life Science, Yangtze University, Jingzhou 434025, China – sequence: 5 givenname: Kamil surname: Musilek fullname: Musilek, Kamil organization: Department of Chemistry, Faculty of Science, University of Hradec Kralove, Hradec Králové 500 03, Czech Republic – sequence: 6 givenname: Eugenie surname: Nepovimova fullname: Nepovimova, Eugenie organization: Department of Chemistry, Faculty of Science, University of Hradec Kralove, Hradec Králové 500 03, Czech Republic – sequence: 7 givenname: Qinghua surname: Wu fullname: Wu, Qinghua email: wqh212@hotmail.com organization: College of Life Science, Yangtze University, Jingzhou 434025, China – sequence: 8 givenname: Wenda surname: Wu fullname: Wu, Wenda email: wuwenda@njau.edu.cn organization: Department of Chemistry, Faculty of Science, University of Hradec Kralove, Hradec Králové 500 03, Czech Republic – sequence: 9 givenname: Vojtech surname: Adam fullname: Adam, Vojtech email: vojtech.adam@mendelu.cz organization: Department of Chemistry and Biochemistry, Mendel University in Brno, Brno 613 00, Czech Republic |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34450232$$D View this record in MEDLINE/PubMed |
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| Keywords | lncRNAs VEGFR2 lncRNA GDEs HIF-1α HIFs PKD3 CXCL-10 S1P TAMs Th DCs CCL5 GSC PGRN PD-L1 PD-L2 MM CD PGE2 IL Tumor microenvironment Tregs STAT3 Bcl Immune evasion EMT FOXP3 TME HMBOX1/SOCS1 MDSCs SLTCL Bregs Mcl miR Hypoxia NK PD-1 BMSCs FGFR2 B7-H4 IDO1 |
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| SubjectTerms | Animals Cell Line, Tumor Humans Hypoxia Immune evasion lncRNA Signal Transduction STAT3 STAT3 Transcription Factor - metabolism Tumor Escape Tumor Microenvironment |
| Title | Signal transducer and activator of transcription 3 signaling in tumor immune evasion |
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