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Dryad

YY1 enhances HIF-1α stability in tumor-associated macrophages to suppress anti-tumor immunity of prostate cancer

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Jun 06, 2025 version files 234.78 MB

Abstract

Prostate cancer, as an immune-cold tumor, shows poor response to immune checkpoint inhibitors, but the underlying mechanisms are not fully understood. Through YY1 proteomics experiments and RNA sequencing of THP-1 cells overexpressing YY1, combined with other biomolecular experiments, we demonstrated that hypoxia promotes the phosphorylation of YY1, thereby enhancing its binding to NUSAP1 and stabilizing HIF-1α, which in turn regulates the tumor microenvironment. Through bioinformatics techniques and in vitro protein IP experiments, we clarified that in tumor-associated macrophages, Tenapanor can competitively bind to the site to block the interaction between YY1 and NUSAP1, thereby affecting the stability of HIF-1α. To verify the therapeutic effects and mechanisms of Tenapanor on prostate cancer, we used the prostate cancer cell line RM1 to induce subcutaneous tumors in C57BL/6 mice. One week after tumor implantation, we administered TEN-M2pep or NC-M2pep (Tenapanor or control solvent linked to TAM-targeting peptide M2pep) via tail vein injection to the experimental group (n=3) and control group mice (n=3). After 24 days, we harvested the subcutaneous tumors, ground them, and digested them into single-cell suspensions. We then performed bulk RNA sequencing on the CD45-selected cells. Additionally, to degrade YY1, we constructed YY1-targeted tetrahedral DNA-caged PROTACs (YY1-DcTACs) and performed single-cell sequencing on subcutaneous tumors from mice injected with YY1-DcTACs and NC-DcTACs via tail vein injection. The combination of both sequencing results, along with further studies using immunohistochemistry and flow cytometry, demonstrated that inhibiting the YY1-NUSAP1 interaction or targeting the degradation of YY1 can promote T cell proliferation and activation, as well as the enrichment of immune response-related pathways in subcutaneous tumors, and enhance the infiltration of CD8+ T cells. These research findings demonstrate that targeting macrophage YY1 is a potential therapeutic strategy for treating prostate cancer and promoting tumor immunity.