Increased expression of focal adhesion kinase correlates with cellular proliferation and apoptosis during 4-nitroquinoline-1-oxide-induced rat tongue carcinogenesis.

摘要

BACKGROUND: Oral carcinogenesis is a multistep process and requires accumulation and interplay of a series of molecular genetic events. Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that plays an important role in signalling pathways that are initiated at sites of integrin-mediated cell adhesions and by growth factor receptors. Overexpression of FAK has been linked to oral squamous cell carcinoma (OSCC). So, it is hypothesized that FAK expression might contribute to oral carcinogenesis. METHODS: During 4-nitroquinoline-1-oxide-induced rat tongue carcinogenesis, FAK protein expression, proliferating cell nuclear antigen (PCNA) and apoptotic nuclei (TUNEL assay) were examined by means of immunohistochemistry. RESULTS: Along with the progress of multistage carcinogenesis, FAK expression increased significantly among different histopathological groups with normal mucosa, mild-dysplastic epithelia, moderate-dysplastic epithelia, severe-dysplastic epithelia and in turn OSCC. Furthermore, FAK immunohistochemical index and PCNA-labelling index displayed positive correlation (r = 0.946, P < 0.05), while negative associations were revealed between apoptotic index and final FAK index (r = -0.959, P < 0.05). CONCLUSION: Our results implicated a role for FAK in oral carcinogenesis. Inhibition of FAK might be a potential novel treatment strategy in this disease.