Se Eun Han1, Chan Ho Park1, Il Sung Nam-Goong1, Young Il Kim1, Eun Sook Kim2. 1. Department of Internal Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Republic of Korea. 2. Department of Internal Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Republic of Korea hanseeun0521@gmail.com endo10@daum.net.
Abstract
BACKGROUND/AIM: The aim of the study was to evaluate the anticancer effects of baicalein in FRO anaplastic thyroid cancer (ATC) cells. MATERIALS AND METHODS: FRO cells were treated with baicalein and viability was measured by the MTT assay. Cell apoptosis was observed by staining with Hoechst dye. The expression of apoptotic proteins (Bax, Bcl-2, PARP, cytochrome c, and caspase-3) and the inflammatory protein Cox-2 and the phosphorylation of MAPKs and Akt were determined by western blot. RESULTS: Treatment with baicalein inhibited cell proliferation in a time-dependent manner and increased DNA fragmentation and apoptosis in FRO cells. Baicalein at 50 and 100 μM inhibited the expression of Bax, PARP, cytochrome c, cleaved caspase-3, and Cox-2, and increased the expression of Bcl-2. Baicalein increased the phosphorylation of ERK, p38 MAPK, and Akt and decreased JNK phosphorylation. CONCLUSION: Baicalein caused anticancer effects in FRO ATC cells through induction of apoptosis and regulation of the MAPK and Akt pathway. Copyright
BACKGROUND/AIM: The aim of the study was to evaluate the anticancer effects of baicalein in FRO anaplastic thyroid cancer (ATC) cells. MATERIALS AND METHODS: FRO cells were treated with baicalein and viability was measured by the MTT assay. Cell apoptosis was observed by staining with Hoechst dye. The expression of apoptotic proteins (Bax, Bcl-2, PARP, cytochrome c, and caspase-3) and the inflammatory protein Cox-2 and the phosphorylation of MAPKs and Akt were determined by western blot. RESULTS: Treatment with baicalein inhibited cell proliferation in a time-dependent manner and increased DNA fragmentation and apoptosis in FRO cells. Baicalein at 50 and 100 μM inhibited the expression of Bax, PARP, cytochrome c, cleaved caspase-3, and Cox-2, and increased the expression of Bcl-2. Baicalein increased the phosphorylation of ERK, p38 MAPK, and Akt and decreased JNK phosphorylation. CONCLUSION:Baicalein caused anticancer effects in FRO ATC cells through induction of apoptosis and regulation of the MAPK and Akt pathway. Copyright