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Nanostring nCounter Mouse PanCancer Immune Profiling analysis of murine tumor tissues

ABSTRACT: The immunosuppressive tumor microenvironment (TME) contributes to resistance against checkpoint inhibitors. However, the precise factors that shape the immune contexture of the TME remain elusive. Here, we report that Single-Stranded DNA Binding Protein 4 (SSBP4), a previously uncharacterized protein, suppresses intratumoral T-cell activation by promoting excessive cholesteryl ester production in tumor cells. Overexpression of SSBP4 in tumor cells decreased T-cell infiltration and accelerated tumor growth in murine syngeneic tumor models. Conversely, genetic ablation of SSBP4 in tumor cells enhanced T-cell infiltration and inhibited tumor growth in a CD8+ T cell–-dependent manner. Mechanistically, SSBP4 upregulated cholesterol synthesis genes, leading to increased production of cholesterol and cholesteryl esters in tumor cells, which directly suppressed CD8+ T-cell activation and function. Furthermore, SSBP4 abrogation significantly improved the efficacy of anti-PD-1 treatment. Thus, in this study, we have identified SSBP4 as a cancer cell–intrinsic regulator of cholesterol metabolism that contributes to tumor immune evasion. Immune-related gene expression was quantified using the Nanostring Mouse PanCancer Immune Profiling panel. Total RNA was isolated from the C57BL/6 SSBP4-wildtype or knockout B16F10 tumors on Day 15 post tumor inoculation. RNA was hybridized, scanned on a Nanostring Digital Analyzer, and raw RCC files were generated. Raw count data were processed and normalized in nSolver or ROSALIND software for downstream immune transcriptome profiling.

ORGANISM(S): Mus musculus

PROVIDER: GSE329266 | GEO | 2026/04/30

REPOSITORIES: GEO

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