非编码RNA（ncRNA）因其在肿瘤发生和进展中的重要作用而受到广泛关注，特别是在免疫治疗耐药中。肿瘤免疫治疗耐药是阻碍肿瘤治疗效果的关键因素，这在很大程度上归因于肿瘤微环境的免疫抑制特性。目前的研究表明，癌症来源的ncRNA通过多种方式参与肿瘤免疫抑制微环境（TIME）的形成。它们不仅促进癌细胞表面免疫检查点配体（例如 PD-L1、CD47、Gal-9 和 CD276）的表达，而且还增强免疫抑制细胞因子（例如 TGF-β、IL-6、 IL-10、VEGF 和趋化因子）。癌症来源的ncRNA还可以通过细胞外囊泡转移到周围的免疫相关细胞中，从而抑制CD8 T细胞和NK细胞的细胞毒性，抑制DC介导的抗原呈递，诱导TAM和CAF的免疫抑制表型转化，增强免疫抑制能力。 Tregs 和 MDSC 的免疫抑制功能。在此，我们总结了癌症来源的 ncRNA 在调节 TIME 形成中的作用，并进一步探索它们作为预后生物标志物和免疫治疗靶点的潜在应用，这将有助于我们在未来解决 TIME 介导的免疫治疗耐药性。本文分类如下：疾病和发育中的 RNA > 疾病调节 RNA/RNAi/核糖开关中的 RNA > 调节 RNA。© 2023 Wiley periodicals LLC。

Non-coding RNAs (ncRNAs) have attracted extensive attention due to their vital roles in tumorigenesis and progression, especially in the immunotherapy resistance. Tumor immunotherapy resistance is a crucial factor hindering the efficacy of tumor treatments, which can be largely attributed to the immunosuppressive properties of tumor microenvironment. Current studies have revealed that cancer-derived ncRNAs are involved in the formation of tumor immunosuppressive microenvironment (TIME) through multiple ways. They not only promote the expression of immune checkpoint ligands (e.g., PD-L1, CD47, Gal-9, and CD276) on cancer cell surfaces, but also enhance the secretion of immunosuppressive cytokines (e.g., TGF-β, IL-6, IL-10, VEGF, and chemokines). Cancer-derived ncRNAs could also be transferred into surrounding immune-related cells through extracellular vesicles, thereby inhibiting the cytotoxicity of CD8+ T cells and NK cells, restraining the DC-mediated antigen presentation, inducing the immunosuppressive phenotype transformation of TAMs and CAFs, and enhancing the immunosuppressive functions of Tregs and MDSCs. Herein, we summarize the roles of cancer-derived ncRNAs in regulating TIME formation and further explore their potential applications as prognostic biomarkers and immunotherapeutic targets, which will help us to address the TIME-mediated immunotherapy resistance in the future. This article is categorized under: RNA in Disease and Development > RNA in Disease Regulatory RNAs/RNAi/Riboswitches > Regulatory RNAs.© 2023 Wiley Periodicals LLC.