The effect of TGF-β on esophageal carcinoma cell lines

• Main Authors: Chia-Yu Yang, 楊佳郁
• Other Authors: Fen-Hwa Wong
• Format: Others
• Language: zh-TW
• Published: 2001
• Online Access: http://ndltd.ncl.edu.tw/handle/74396459641577460318

碩士 === 國立陽明大學 === 公共衛生研究所 === 89 === Transforming growth factor-βs (TGF-βs) are multifunctional growth factors that inhibit the growth of most epithelial cells. In this study, we investigated the biological effects of TGF-β on esophageal carcinoma cells. In esophageal carcinoma cell lines, CE146T/VGH, TGF-β treatment accelerated its proliferation. While in the other cell line, CE81T/VGH, treatment with 1 ng/ml TGF-β inhibit cell-cycle progression by arresting cells in G1 phase, but with 8 ng/ml TGF-β accelerated cell proliferation. The mechanism by which TGF-β induced different biological effects in two esophageal carcinoma cell lines needs more studies. We also fined that treatment CE81T/VGH with 1 ng/ml TGF-β induces G1 arrest through the down regulation of Cyclin D and CdK4, but not of Cyclin E, CdK2, or p21. Treatment CE81T/VGH with 1 ng/ml TGF-β also decreased the protein level of Survivin, a human IAP protein. Proteasome inhibitor can block Survivin decreasing induced by TGF-β, suggest that Survivin is degraded by the ubiquitin-proteasome pathway. To address the role of Survivin in cell cycle arrest, we transfected the human survivin in the CE81T/VGH cells. Overexpression of survivin did not overcome TGF-β induced G1 arrest. The biological effect of TGF-β induced Survivin degradation needs further studies.