Estabishment of G0 cancer cell model for the development of therapeutic strategy to target seceding from and re-entry into cell cycle in cancer cell

我们已经发现，胰腺癌细胞在缺氧条件下的增殖受到抑制，并且Hedgehog信号在缺氧条件下被激活。从而提出Hedgehog信号通路可能参与细胞从G 0/G1期重新进入细胞周期的机制。为了分析这一机制，我们已经产生了耐缺氧的胰腺癌细胞系，并已证实Hedgehog信号，特别是Smo分子是参与从G 0/G1期重新进入细胞周期的机制之一，通过在体外和体内实验中再给这种耐缺氧的细胞系供氧。

We have found that proliferation in pancreatic cancer cells under hypoxia is inhibited and that Hedgehog signaling is activated under hypoxia. Then we have provided the possibility that Hedgehog signaling may contribute to the mechanism of the re-entry into cell cycle from G0/G1 phase. To analyze this mechanism we have generated the hypoxia-resistant pancreatic cancer cell line and have confirmed that Hedgehog signaling, especially Smo molecule is involved in one of the mechanisms of re-entry into cell cycle from G0/G1 phase by reoxygenating this hypoxia-resistant cell line in vitro and in vivo experiments.