Eischen Christine M, Lozano Guillermina
Department of Pathology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
Cancer Cell. 2009 Mar 3;15(3):161-2. doi: 10.1016/j.ccr.2009.02.004.
Therapeutics that disrupt the p53-MDM2 interaction show promise for cancer treatment but surprisingly have different biological outcomes. A study by Enge et al. in this issue of Cancer Cell shows that the ability of MDM2 to target hnRNP K for degradation contributes to the decision to induce apoptosis rather than cell-cycle arrest.
破坏p53-MDM2相互作用的疗法在癌症治疗方面显示出前景,但令人惊讶的是会产生不同的生物学结果。恩格等人在本期《癌细胞》上发表的一项研究表明,MDM2将异质性核糖核蛋白K(hnRNP K)靶向降解的能力有助于决定诱导细胞凋亡而非细胞周期停滞。