Abstract
CD73 is a cell surface immunosuppressive enzyme involved in tumor progression and metastasis. While patients whose cancer cells express elevated CD73 are typically associated with an unfavorable outcome, the clinical impact of CD73 expression in patients with Head and neck squamous cell carcinoma (HNSCC) remains unclear. In the present study, we investigated the prognostic significance of CD73 in HNSCC using gene and protein expression analyses. Our results demonstrate that high levels of CD73 are significantly associated with reduced overall survival in patients with HNSCC. We also investigated the functional role of CD73 in vitro and demonstrated that CD73 promotes HNSCC migration and invasion through adenosine A3R stimulation and the activation of EGF/EGFR signaling. Moreover, in vivo xenograft studies demonstrated that CD73 promotes tumorigenesis. In conclusion, our study highlights a role for CD73 as a poor prognostic marker of patient survival and also as a candidate therapeutic target in HNSCCs.
Highlights
Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer in the world, accounting for nearly 3% of all cancers
Quantification analysis revealed that CD73 expression in epithelial dysplasia and HNSCC is strongly positive as compared to the normal oral mucosa (P < 0.05 and P < 0.001, Figure 1B)
While no difference was observed between different Grades or T categories, we did identify a statistically significant difference between CD73 expression in specimens with lymph node metastasis (N+) and versus those where lymph node metastasis was not observed (N−)
Summary
Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer in the world, accounting for nearly 3% of all cancers. HNSCC is the most common and lethal histopathological type of head and neck cancer with a 5-year survival rate of about 50% [1, 2]. Despite significant research advances in our understanding of the prevention, diagnostics, and treatment strategies for this disease, the survival rate of patients with HNSCC has shown minimal improvements [4,5,6,7,8,9,10]. The development of novel therapies and improved understanding of the mechanisms underlying HNSCC invasion and metastasis represent issues of critical, clinical significance
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