非典型畸胎样/横纹肌样瘤中mir-221和mir-222的上调：潜在的治疗靶点。
Upregulation of mir-221 and mir-222 in atypical teratoid/rhabdoid tumors: potential therapeutic targets.
作者信息
Sredni Simone Treiger, Bonaldo Maria de Fátima, Costa Fabrício Falconi, Huang Chiang-Ching, Hamm Christopher Allan, Rajaram Veena, Tomita Tadanori, Goldman Stewart, Bischof Jared Marshall, Soares Marcelo Bento
机构信息
Cancer Biology and Epigenomics Program, Children's Memorial Research Center, Department of Pediatrics, Feinberg School of Medicine, Children's Memorial Hospital, 2300 Children's Plaza, Chicago, IL 60614, USA.
出版信息
Childs Nerv Syst. 2010 Mar;26(3):279-83. doi: 10.1007/s00381-009-1028-y. Epub 2009 Dec 10.
PURPOSE
The aim of this study is to search for new therapeutic targets for atypical teratoid-rhabdoid tumors (ATRT).
METHODS
To achieve this, we compared the expression of 365 microRNAs among ATRT, medulloblastomas, and normal brain.
RESULTS
MiR-221 and miR-222 were within the top differentially expressed microRNAs. The deregulated expression of miR221/222 was demonstrated to inhibit the expression of the tumor suppressor and inhibitor of cell cycle p27(Kip1). Here, we demonstrated the negative regulation of p27(Kip1) by miR-221/222 in ATRT using microarray, real-time reverse transcriptase polymerase chain reaction, and immunohistochemistry.
CONCLUSION
As anti-miR therapy was recently proposed as an alternative treatment for cancer, these findings suggest that anti-miR-221/222 therapy might have therapeutic potential in ATRT.
目的
本研究旨在寻找非典型畸胎样横纹肌样肿瘤（ATRT）的新治疗靶点。
方法
为实现这一目标，我们比较了ATRT、髓母细胞瘤和正常脑组织中365种微小RNA的表达情况。
结果
MiR-221和MiR-222位列差异表达最显著的微小RNA之中。已证实MiR221/222的失调表达会抑制肿瘤抑制因子及细胞周期抑制剂p27（Kip1）的表达。在此，我们运用微阵列、实时逆转录聚合酶链反应及免疫组化方法，证明了在ATRT中MiR-221/222对p27（Kip1）的负调控作用。
结论
鉴于抗微小RNA疗法最近被提议作为癌症的一种替代治疗方法，这些发现表明抗MiR-221/222疗法在ATRT中可能具有治疗潜力。
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