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 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 tumormicroenvironment (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 alpha, exosome, lncRNA, and autophagy in the promotion of tumor immune evasion and highlighted the recent research on STAT3 signaling and tumor immune evasion thatmay assist in developing effective STAT3-targeted drugs for advancing immunotherapy. (C) 2021 Elsevier Inc. All rights reserved.

Automated summary

The underlying mechanism of tumor immune evasion, particularly the role of STAT3 in promoting tumor cell escape from immune surveillance through regulating autophagy molecules, immune factors, and immunosuppressive cell recruitment, is discussed in this review. The article also highlights the significance of the research on STAT3 signaling and tumor immune evasion in the development of targeted drugs for immunotherapy.