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| 1 | 抑癌基因与癌基因的最新研究进展显示文摘正常情况下,抑癌基因通过抑制细胞周期,促进细胞衰老,或促进细胞凋亡来监控细胞状态,防止细胞异常增殖。相反,癌基因则是通过使细胞逃逸周期抑制,促进细胞异常增殖,阻止细胞凋亡,从而导致细胞癌变。但是,在不同细胞背景或基因突变状态下,抑癌基因可能转变为癌基因的功能,反之亦然。 | 李海丽 邵驰浩 周若宇 张永进 李翠 罗瑛 | 2018 | 基础医学与临床2018，38，7： | 12 |
| 2 | Sirt3 is critical for p53-mediated ferroptosis upon ROS-induced stress显示文摘Dear Editor,p53 acts as a transcription factor to modulate various types of cellular processes to suppress tumor development(Tackmann and Zhang,2017).The exquisite regulation of p53 functions is of vital importance for cell fate decisions.Although it is well accepted that p53-mediated cell-cycle arrest,senescence,and apoptosis serve as major tumor suppression mechanisms,recent studies suggest that other unconventional activities such as ferroptosis are also critically involved in its tumor suppressor function(Li et al.,2012).We and others found that p53 plays an important role in modulating ferroptotic responses through its metabolic targets(Jiang et al.,2015;Jennis et al.,2016;Wang et al.,2016).Ferroptosis is a regulated form of iron-dependent,non-apoptotic cell death characterized by excessive reactive oxygen species(ROS)generation and accumulation of lipid peroxidates(Stockwell et al.,2020).Lipid peroxides are normally eliminated by glutathione peroxidase 4(GPX4)and its co-factor glutathione(GSH),which convert lipid hydroperoxides to non-toxic lipid alcohols.Thus,ferroptosis can be artificially induced by pharmacological agents that disrupt this lipid repair system,allowing lethal accumulation of lipid peroxides.Such agents include direct GPX4 enzymatic inhibitors,as well as the small molecule erastin,which suppress glutathione synthesis and indirectly suppress GPX4 activation(Stockwell et al.,2020).Although activation of p53 expression is able to modulate ferroptosis induced by GPX4 inhibition in certain cell types(Jiang et al.,2015),p53-mediated ferroptotic responses are also observed upon ROS-induced stress,apparently through a GPX4-independent manner(Chu et al.,2019).Nevertheless,the molecular factors that modulate p53-dependent ferroptosis upon ROS stress need further elucidation.Sirt3 is a NAD-dependent deacetylase predominantly localized in mitochondria,which functions in multiple metabolic pathways,including electron transport chain,fatty acid oxidation,amino acid metabolism,redox balance,and the tricarboxylic acid(TCA)cycle(Van de Ven et al.,2017).Here,we identified Sirt3 as a novel repressor in p53-mediated ferroptosis induced by ROS stress. | Ying Jin Wei Gu Weichang Chen | 2021 | Journal of Molecular Cell Biology2021，13，2： | 3 |
| 3 | 主动脉夹层中层P53、MDM2及TRIM25的表达变化和VSMC表型转化显示文摘目的探讨主动脉中层中α-SMA、OPN、P53、MDM2和TRIM25蛋白在主动脉夹层中的表达变化及其意义。方法将12例A型AD手术患者的升主动脉作为实验组,12例DCD供体的升主动脉作为对照组。用免疫组化和Western blot法检测α-SMA、OPN、P53、MDM2、TRIM25和p-P53在AD组及对照组中的表达情况,用RT-PCR技术检测AD组及对照组组织中P53、MDM2及TRIM-25mRNA含量。结果通过Western blot法和RT-PCR法检测结果显示,P53、MDM2和TRIM-25的蛋白、mRNA含量在AD组织中明显增加,免疫组化检测也表明P53、MDM2和TRIM25含量增加,但其p-P53水平却下降。免疫组化结果显示α-SMA阳性细胞在AD组中的含量较对照组显著减少,而OPN阳性细胞在AD组增高,进一步Western blot法检测也证实了这一变化。结论 AD主动脉中层中VSMC表型向去分化型转变,而P53、MDM2、TRIM25的表达量增高,提示TRIM25可能通过影响P53/MDM2反馈环而导致VSMC表型转变参与AD形成。 | 任伟 王志维 李博文 昌金星 王嘉慧 | 2019 | 医学研究杂志2019，48，2： | 2 |
| 4 | 羽扇豆醇介导MDM2-p53通路对胃癌细胞生物学行为的影响显示文摘目的:探讨羽扇豆醇介导鼠双微基因2(Mouse double microgene 2,MDM2)-p53通路对胃癌细胞生物学行为的影响及相关机制。方法:对数生长期的胃癌小鼠MFC细胞株随机分为三组。实验1组与实验2组给予10 mg/L和20 mg/L的羽扇豆醇处理,对照组以等体积的1×磷酸盐缓冲液处理。对比三组MFC细胞细胞增殖、凋亡、迁移与侵袭,及MDM2-p53通路蛋白表达。结果:细胞处理后6 h与12 h,实验1组与实验2组的细胞增殖指数、细胞迁移与侵袭指数、MDM2蛋白相对表达水平显著低对于对照组,实验2组也低于实验1组,对比差异都有统计学意义(P<0.05)。细胞处理后6 h与12 h,实验1组与实验2组的细胞凋亡指数、p53蛋白相对表达水平显著高于对照组,实验2组也高于实验1组,对比差异都有统计学意义(P<0.05)。结论:羽扇豆醇能促进胃癌细胞p53蛋白的表达,抑制MDM2蛋白的表达,从而促进细胞凋亡,抑制胃癌的增殖、侵袭与转移,且具有剂量依赖性。 | 吴元元 费素娟 苗蓓 赵锛活 李桃 | 2021 | 现代生物医学进展2021，21，1： | 2 |
| 5 | What's knowledge is prologue:celebrating the 40th anniversary of the p53 discovery显示文摘It is my great honor to deliver a welcome speech as the Editor-in-Chief of Journal of Molecular Cell Biology (JMCB) and the Chair of JMCB Symposium 2019:The Legend of p53 vs.Cancer.Please allow me to borrow the logion 'what's past is prologue' from the great English playwright William Shakespeare as follows. | | 2019 | Journal of Molecular Cell Biology2019，11，7： | 1 |
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