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
Statistics from Altmetric.com
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.
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.