Signal transducer and activator of transcription 3 signaling in tumor immune evasion
Open accessAbstract
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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STAT3 constitutively occupies the proximal region of the PD-L1 promoter and directly regulates PD-L1 expression.
“On the other hand, STAT3 constitutively occupies the proximal region of the PD-L1 promoter and directly regulates PD-L1 expression (36).”
From Small-molecule PROTAC mediates targeted protein degradation to treat STAT3-dependent epithelial cancer (2022) · cites this paper as [36]
Engagement of PD-L1 and PD-1 exerts inhibitory effects on T cells by inducing their apoptosis and anergy.
“The engagement of PD-L1 and PD-1 exerts inhibitory effects on T cells by inducing their apoptosis and anergy (36).”
From Small-molecule PROTAC mediates targeted protein degradation to treat STAT3-dependent epithelial cancer (2022) · cites this paper as [36]
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- Authors
- Zhang, L., Kuca, K., You, L., Zhao, Y., Musilek, K., Nepovimova, E., Wu, Q., Wu, W., & Adam, V.
- Affiliations
- Yangtze University (CN)
- Nanjing Agricultural University (CN)
- Corresponding author
- Wu, Qinghua
- Wu, Wenda
- Venue
- Pharmacology & Therapeutics
- Publisher
- Elsevier BV
- Published
- 2022-02
- Volume
- 230
- Pages
- 107969
- ISSN
- 0163-7258 (ISSN-L)
- OpenAlex
- W3194006508
- Cited by
- 67
- References
- 110
- Citations by year
- 2026: 11 · 2025: 16 · 2024: 13 · 2023: 14 · 2022: 13
- FWCI
- 1.21
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- Locations
- Pharmacology & Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- Brno University of Technology Digital Library (Brno University of Technology) (acceptedVersion, cc-by-nc-nd)
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Keywords
- STAT3 signaling, tumor immune evasion, tumor microenvironment, PD-L1, HIF-1α, exosomes, long non-coding RNA, autophagy, CTL-mediated lysis, natural killer cells, T cell apoptosis, immunosuppression, cancer immunotherapy
- MeSH terms
- Animals, Humans, Signal Transduction, Tumor Escape, Cell Line, Tumor, STAT3 Transcription Factor, Tumor Microenvironment
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