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

ABSTRACT: The ?-3 fatty acid desaturase (fat-1) gene encodes the enzyme that converts ?-6 polyunsaturated fatty acids (PUFAs) to ?-3 PUFAs. Numerous studies have suggested that the ratio of ?-6/?-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 ?-3/?-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 ?-catenin. The results also support the theory that the ratio of ?-3/?-6 PUFAs has an impact on OSCC tumor growth. The findings of the study provide notable molecular insight into the theory suggesting that ?-3 PUFAs are an intermediate for the chemoprevention and treatment of human OSCC.

SUBMITTER: Nie D 

PROVIDER: S-EPMC4726880 | biostudies-literature | 2016 Jan

REPOSITORIES: biostudies-literature