Cellular and microenvironmental functions of SNHG lncRNAs in tumor immune remodeling

The dynamic interplay between tumor cells and immune components within the tumor microenvironment (TME) is a critical determinant of cancer progression. At the tissue and cellular levels, immune surveillance mechanisms mediated by cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells are responsible for recognizing and eliminating transformed cells. However, tumor cells remodel their microenvironment to establish an immunosuppressive niche that supports immune evasion. Increasing evidence identifies long non-coding RNAs (lncRNAs), particularly members of the small nucleolar RNA host gene (SNHG) family, as key regulators of tumor-immune cell interactions. This review focuses on the cellular and tissue-specific mechanisms by which SNHG lncRNAs (including SNHG1, SNHG3, SNHG4, SNHG9, SNHG10, SNHG12, SNHG14, SNHG15, SNHG17 and SNHG20) modulate the immune landscape across diverse malignancies. Mechanistically, SNHGs function through competitive endogenous RNA (ceRNA) networks, signaling pathway modulation, and epigenetic regulation to influence immune cell differentiation and activity within the TME. They promote regulatory T cell (Treg) expansion, drive macrophage polarization toward the M2 phenotype, suppress NK cell cytotoxicity, impair CTL responses, and enhance expression of immunosuppressive mediators such as PD-L1 and IL-6R. By reshaping immune cell composition and function at the tissue level, SNHG lncRNAs contribute to the establishment of an immunologically permissive tumor niche. Understanding these cellular regulatory circuits highlights SNHG family members as potential modulators of tumor-immune crosstalk and as promising targets for microenvironment-directed therapeutic strategies.