Studies on the involvement of peroxisome-proliferator activated receptor in rat tongue carcinogenesis and inhibition by their ligands

点击翻译按钮获取中文摘要

The present study was conducted to investigate the possible involvement of PPAR expression during tongue carcinogenesis and the chemopreventive ability of PPAR ligands against tongue tumorigenesis in rats. The results obtained are as follows :1) The human tongue cancer cell lines HCS-2 and NA expressed PPARγ and the expression of NA was greater than HCS-2.2) The growth of HCS-2 was inhibited by adding at high doses (40-50 μM) of a PPARγ ligand troglitazone and that of NA was inhibited dose-dependently by adding of troglitazone. FCM analysis revealed that troglitazone caused G1 arrest and apoptosis in both cell lines. The treatment also induced COX-2 expression.3) Dietary troglitazone (100 ppm) significantly inhibited 4-NQO-induced rat tongue carcinogenesis.4) Rat tongue squamous cell carcinoma induced by 4-NQO did not have β-catenin mutation.5) Dietary silymarin, which is an antioxidant and an inhibitor of arachidonic acid cascade, inhibited 4-NQO-induced rat tongue carcinogenesis through inhibition of cell proliferation and PGE2 biosynthesis.6) Apoptosis inducers capsaicin and rotenone from plants inhibited 4-NQO-induced rat tongue carcinogenesis through inhibition of cell proliferation and induction of Phase II drug metabolizing enzymes.