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Published on: November 28, 2019
High SIGLEC10-Expressing Tumor-Associated Macrophages Participate in Remodeling the Tumor Immune Microenvironment and
1Department of General Surgery, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong, China.
Background:
Sialic acid-binding immunoglobulin-like lectin 10 (SIGLEC10), a member of the SIGLEC family, is selectively expressed on multiple immune cell subsets and plays a key role in immune regulation through the recognition of sialylated ligands. Recent studies suggest that SIGLEC10 functions as an emerging immune checkpoint that contributes to the regulation of tumor-associated macrophages (TAMs) within the tumor microenvironment (TME).
Methods:
Immunohistochemistry was performed to assess SIGLEC10 expression in a CRC cohort comprising 202 patients, and the association between SIGLEC10 expression and patient survival and prognosis was evaluated. Immunofluorescence staining and flow cytometry were used to characterize the localization and phenotypic features of SIGLEC10-expressing cells within tumor tissues. The Cancer Genome Atlas (TCGA) and RNA sequencing (RNA-seq) datasets were analyzed to investigate SIGLEC10-associated tumor immune signaling pathways. Additionally, single-cell datasets from Tumor Immune Single-cell Hub 2 (TISCH2) were used to further investigate the regulatory mechanisms of SIGLEC10high TAMs within the TME. Finally, the therapeutic potential of SIGLEC10 as an immunotherapeutic target in CRC was evaluated.
Results:
High SIGLEC10 expression predicts poor prognosis in CRC patients and serves as an independent prognostic factor. SIGLEC10 is predominantly expressed in CD68+ macrophages and is associated with TAMs phenotypes. Functional enrichment analyses indicate that SIGLEC10high TAMs are involved in the regulation of multiple inflammatory and tumor immune signaling pathways. Immune infiltration and differential analyses suggest that SIGLEC10high TAMs may facilitate tumor immune evasion by promoting increased infiltration of immune cells and recruiting various immune chemokines. Single-cell analyses reveal that SIGLEC10high TAMs may remodel the TME through TNFSF13B-mediated regulation of multiple immune cell populations, including B cells. Finally, SIGLEC10 exhibits considerable potential as an immunotherapeutic target for CRC.
Conclusion:
This study highlights SIGLEC10 as an independent prognostic factor in patients with CRC and its potential as a promising target for immunotherapy in CRC.
