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

我们发现胰腺癌细胞在缺氧条件下增殖受到抑制，Hedgehog信号在缺氧条件下被激活。然后，我们提出了刺猬信号可能有助于从G0/G1期重新进入细胞周期的机制。为了分析这一机制，我们制备了耐缺氧胰腺癌细胞系，并通过体外和体内实验证实了Hedgehog信号特别是Smo分子参与了这种耐缺氧细胞系从G0/G1期重新进入细胞周期的机制之一。

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.