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.

肿瘤免疫逃避的潜在机制是研究人员高度关注的课题。越来越多的证据表明，过度激活的信号转导和转录激活因子 3 (STAT3) 是恶性肿瘤的关键分子中枢。STAT3 控制损害 CTL 介导的肿瘤细胞裂解的自噬分子，抑制自然杀伤细胞并诱导 T 淋巴细胞凋亡以创造免疫抑制环境。STAT3 信号调节免疫因子的表达并招募免疫抑制细胞以建立耐受的肿瘤微环境 (TME)。STAT3 信号调节免疫因子的表达并募集免疫抑制细胞以创造免疫抑制环境。所有这些都有助于肿瘤细胞逃避免疫监视。在本次审查中，我们概述了参与肿瘤免疫逃避的 STAT3 介导的机制及其在 TME 中的潜在调节功能。我们讨论了 STAT3 信号对 PD-L1、HIF-1α、外泌体、lncRNA 和自噬在促进肿瘤免疫逃避中的影响，并强调了最近关于 STAT3 信号和肿瘤免疫逃避的研究可能有助于开发有效的 STAT3 靶向用于推进免疫治疗的药物。