Aims Galectin-1 (Gal-1) is a β-galactoside-binding protein that overexpresses in cancer and plays pivotal roles in tumour progression. Gal-1 regulates angiogenesis and invasiveness, and suppresses tumour immunity by inducing T cell apoptosis. Several studies have examined the relationship between Gal-1 and tumour immunosuppression in vivo, but they have not examined the clinicopathological relationship between Gal-1 expression and apoptotic T cell number in human tissue. In this study, we investigated the association between Gal-1 expression and apoptotic T cells of gingival squamous cell carcinoma (GSCC), as well as other clinicopathological factors.
Methods Immunohistochemical investigation of 80 GSCC specimens using anti-Gal-1, anti-CD3, anti-CD4, anti-CD8, anti-CD34, antipodoplanin and anticleaved caspase-3 (CC-3) antibodies was performed. Relative expression levels of CD3 and CC-3, as well as CD8 and CC-3 were assessed simultaneously by double immunostaining. Gal-1 expression and T cell apoptosis were evaluated in 6 high-power fields (3 in the tumour and 3 in the stroma).
Results Gal-1 expression in GSCC was significantly correlated with T cell infiltration (p=0.036), and apoptosis of CD3+ and CD8+ T cells (p<0.001). Moreover, Gal-1 expression was significantly correlated with lymph node metastasis (p=0.021), histological differentiation (p<0.001) and overall survival rate (p=0.021).
Conclusions These findings suggest that Gal-1 plays an important role in immune escape of GSCC cells, and Gal-1 expression level may be a useful clinicopathological prognostic marker for GSCC.
- ORAL PATHOLOGY
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Handling editor Cheok Soon Lee
Contributors Study concepts and study design: YN and MK. Data acquisition: YN, MK, YF and SM. Quality control of data and algorithms: YN, MK, KH and MS. Data analysis and interpretation: YN, MK, SS and ST. Statistical analysis: YN, MK and SS. Manuscript preparation: YN and MK. Manuscript editing and manuscript review: YN, MK and ST.
Funding This study was supported by Grants-in-Aid for Scientific Research, Japan Society for the Promotion of Science (C254628520).
Competing interests None declared.
Ethics approval Institutional Review Board of Osaka University Graduate School of Dentistry (H27-E15).
Provenance and peer review Not commissioned; externally peer reviewed.