| Summary: | 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.
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