肿瘤抑制因子程序性细胞死亡蛋白4（PDCD4）及其拮抗物致癌性微小RNA-21（miR-21）是否失控了？
Have tumor suppressor PDCD4 and its counteragent oncogenic miR-21 gone rogue?
作者信息
Young Matthew R, Santhanam Arti N, Yoshikawa Noriko, Colburn Nancy H
机构信息
Laboratory of Cancer Prevention, Center for Cancer Research, National Cancer Institute, Frederick, MD, 21702, USA.
出版信息
Mol Interv. 2010 Apr;10(2):76-9. doi: 10.1124/mi.10.2.5.
A recent article suggests that the well known tumor suppressor PDCD4 also functions as a pro-inflammatory agent. The PDCD4 counteragent miR-21, a pro-oncogenic micro-RNA, is described as an anti-inflammatory agent. The authors of this research article provide evidence that mice lacking PDCD4 are protected from the lethal effects of lipopolysaccharide (LPS). This report also confirms miR-21 as a negative regulator of PDCD4 expression after LPS stimulation. Downstream mediators of the pro-inflammatory activity of PDCD4 include IL-10, an anti-inflammatory cytokine that is negatively regulated by PDCD4, and IL-6, a pro-inflammatory cytokine that appears to be upregulated in a PDCD4 dependent manner, possibly through an increase in NF-κB activity. Is it possible that a tumor-suppressor protein and an oncogenic micro-RNA can be oppositely targeted to control inflammatory disease?
最近一篇文章表明，著名的肿瘤抑制因子PDCD4也具有促炎因子的功能。PDCD4的拮抗物miR-21是一种促癌微小RNA，被描述为一种抗炎因子。这篇研究文章的作者提供证据表明，缺乏PDCD4的小鼠可免受脂多糖（LPS）的致死作用。该报告还证实，miR-21是LPS刺激后PDCD4表达的负调节因子。PDCD4促炎活性的下游介质包括IL-10（一种抗炎细胞因子，受PDCD4负调节）和IL-6（一种促炎细胞因子，似乎以PDCD4依赖的方式上调，可能是通过NF-κB活性的增加）。一种肿瘤抑制蛋白和一种致癌微小RNA有可能被反向靶向以控制炎症性疾病吗？
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