Association of NCCRP1 expression with T category and in vitro growth-related characteristics of head and neck squamous cell carcinoma FaDu cells

Abstract

Nonspecific cytotoxic cell receptor protein 1 (NCCRP1), which is expressed in normal squamous epithelium, has been reported as a prognostic marker for esophageal squamous cell carcinoma and triple-negative breast cancer. Here, we evaluated expression of NCCRP1 in head and neck squamous cell carcinoma (HNSCC) and adjacent normal mucosa, its association with clinicopathological features, and in vitro growth-related characteristics following forced NCCRP1 expression. In the present study, we evaluated expression levels of NCCRP1 in formalin-fixed, paraffin-embedded samples of specimens collected by biopsy and resection from 43 patients with HNSCC and examined association of NCCRP1 expression with clinicopathological characteristics. Human HNSCC FaDu cells with forced NCCRP1 expression were assessed using the MTT assay and the colony formation assay. We found that NCCRP1 was expressed in noncancerous spinosum and superficial epithelial layers of the oral cavity, nasopharynx, mesopharynx, hypopharynx, and larynx. NCCRP1 expression in HNSCC tissues showed considerable variation, contrasting to relatively uniform expression in noncancerous surrounding mucosa. Based on NCCRP1 staining proportion in tumor, 31 of the 43 patients (72.1%) were classified as NCCRP1-low and the remaining 12 (27.9%) patients as NCCRP1-high. NCCRP1 expression in HNSCC tissue showed an exploratory association with T category (p = 0.0215). HNSCC FaDu cells with forced NCCRP1 expression exhibited enhanced in vitro growth-related characteristics measured by the MTT and colony formation assays. NCCRP1 expression was associated with T category in this selected HNSCC cohort, and forced NCCRP1 overexpression in FaDu cells was associated with increased in vitro growth-related measurements. Nevertheless, these exploratory findings require validation in independent clinical cohorts and experimental models.