作者: Wensheng Yan , Xinbin Chen
关键词:
摘要: Tumor cells, including SW480 carcinoma cells that carry a mutant p53, are addicted to the for their survival and resistance growth suppression by chemotherapeutic agents. Here, we investigated whether various classes of p53 mutants share common property functional domains necessary gain function. To test this, generated cell lines in which endogenous R273H/P309S can be inducibly or stably knocked down, whereas small interfering RNA-resistant along with mutated domain expressed. We found both contact-site (R248W R273H) conformation (G245S R249S) able maintain transformed phenotypes conferred p53. also activation 1–2 proline-rich required Interestingly, showed C-terminal basic domain, is wild-type activity, an inhibitory Furthermore, deletion enhances, mutation abolish regulate Gro1 Id2, regulated mediate These results indicate transformation, critical tumor promotion. Thus, explored targeting tumors