Department of Biochemistry and Molecular Biology, Virginia Commonwealth University, Richmond, Virginia 23298-0614, USA.
J Clin Invest. 2012 Jan;122(1):16-9. doi: 10.1172/JCI61677. Epub 2011 Dec 27.
Chronic inflammation has long been appreciated to play a critical role in tumor development and maintenance. Among the mechanisms involved in coordinating the initiation and resolution of inflammation are those responsible for modifying mRNA stability and/or translation. Several studies have linked the RNA-binding protein HuR, which increases mRNA stability, with malignant transformation. However, in this issue of the JCI, Yiakouvaki et al. compellingly demonstrate in mice that increased HuR activity in myeloid cells has a protective role in the onset of pathologic intestinal inflammation (i.e., colitis) and colitis-associated cancer (CAC). These observations highlight the need to understand the roles of HuR in distinct cell populations in vivo and suggest that enhancing HuR activity may be of clinical benefit in protecting against pathologic inflammation and cancer.
慢性炎症长期以来被认为在肿瘤的发生和维持中起着关键作用。在参与协调炎症的发生和消退的机制中，有一些机制负责修饰 mRNA 的稳定性和/或翻译。几项研究将 RNA 结合蛋白 HuR 与恶性转化联系起来，HuR 可增加 mRNA 的稳定性。然而，在本期 JCI 中，Yiakouvaki 等人在小鼠中令人信服地证明，髓系细胞中 HuR 活性的增加在病理性肠道炎症（即结肠炎）和结肠炎相关癌症（CAC）的发病中具有保护作用。这些观察结果强调了需要在体内理解 HuR 在不同细胞群体中的作用，并表明增强 HuR 活性可能有助于预防病理性炎症和癌症。
