Wu Ting-He, Yang Ruo-Lin, Xie Li-Ping, Wang Hong-Zhong, Chen Lei, Zhang Shuyi, Zhao Yong, Zhang Rong-Qing
Laboratory of Marine Biotechnology, Department of Biological Science and Biotechnology, Tsinghua University, Beijing 100084, People's Republic of China.
Cancer Lett. 2006 Feb 8;232(2):199-205. doi: 10.1016/j.canlet.2005.02.018.
In this study, we report that the steroid extract 5alpha, 8alpha-epidioxycholest-6-ene-3beta-ol (MME) from Meretrix meretrix has the ability to inhibit growth of hepatoma cells and to induce G1-phase cell cycle arrest in two human hepatoma cell lines, HepG2 and Hep3B. HepG2 cells were more sensitive than Hep3B to MME. The extract markedly up-regulated the expression of p53 and p21WAF1/CIP1 in HepG2, suggesting that MME-induced G1 phase cell cycle arrest in HepG2 might be p53-dependent. Therefore, the up-regulation of p27KIP1and p16INK4A in both cell lines indicates that a p53-independent pathway might be involved in the mechanism of MME inducing cell cycle arrest. In conclusion, MME induces G1 phase cell cycle arrest via both p53-dependent and p53-independent pathways.
在本研究中，我们报告称，来自文蛤的甾体提取物5α, 8α-环氧胆甾-6-烯-3β-醇（MME）具有抑制肝癌细胞生长并诱导两种人肝癌细胞系HepG2和Hep3B的G1期细胞周期停滞的能力。HepG2细胞比Hep3B细胞对MME更敏感。该提取物显著上调了HepG2中p53和p21WAF1/CIP1的表达，这表明MME诱导HepG2细胞的G1期细胞周期停滞可能依赖于p53。因此，两种细胞系中p27KIP1和p16INK4A的上调表明，一条不依赖p53的途径可能参与了MME诱导细胞周期停滞的机制。总之，MME通过依赖p53和不依赖p53的途径诱导G1期细胞周期停滞。
