Fat-1 gene inhibits human oral squamous carcinoma cell proliferation through downregulation of β-catenin signaling pathways

Abstract

The ω-3 fatty acid desaturase (fat-1) gene encodes the enzyme that converts ω-6 polyunsaturated fatty acids (PUFAs) to ω-3 PUFAs. Numerous studies have suggested that the ratio of ω-6/ω‑3 PUFAs has an impact on tumorigenesis. To investigate the biological function of the fat‑1 gene in human oral squamous cell carcinoma (OSCC), the fat‑1 gene was introduced into OSCC cells by transfection. The uptake of the gene was confirmed by reverse transcription‑polymerase chain reaction and analyzed using gas chromatography. The antitumor effects and mechanisms of the fat‑1 gene were evaluated by studying cell survival and tumor growth in vitro and in vivo. Gas chromatography results revealed that the cells transfected with the fat‑1 gene had a higher ω‑3/ω‑6 PUFA ratio than cells transfected with the control vector. An MTT and DNA fragmentation assay indicated that the presence of the fat‑1 gene in vitro significantly decreased OSCC cell proliferation and significantly increased the rate of apoptosis. Similar antitumor effects of the fat‑1 gene were also observed in vivo. Immunohistochemistry analysis confirmed that Tca8113 cell tumors displayed a significant reduction in cell growth and cell survival following the introduction of the fat‑1 gene. The current study suggests that the inhibitory effect of the fat‑1 gene on tumor growth may be a result of a reduction in the expression of the tumor survival protein β‑catenin. The results also support the theory that the ratio of ω‑3/ω‑6 PUFAs has an impact on OSCC tumor growth. The findings of the study provide notable molecular insight into the theory suggesting that ω‑3 PUFAs are an intermediate for the chemoprevention and treatment of human OSCC.