美國科學家近日研究發(fā)現(xiàn),，一種與白血病和肺癌有關的分子,，對于肌修復和一種肌肉癌同樣重要,。相關論文發(fā)表在《癌細胞》（Cancer Cell）雜志上。
俄亥俄州立大學研究人員Denis C. Guttridge和同事發(fā)現(xiàn),，肌細胞需要這一稱為miR-29（一種小分子RNA）的分子以達到成熟狀態(tài),，而來自橫紋肌肉瘤（rhabdomyosarcoma）的細胞中幾乎不存在這種分子，橫紋肌肉瘤是由未成熟肌細胞增殖導致的一種癌癥,。
研究人員發(fā)現(xiàn),，miR-29基因的活性被NF-κB蛋白“沉默”。橫紋肌肉瘤細胞中含有高濃度的這種蛋白,，使得miR-29的作用被切斷,，從而阻止了肌肉祖細胞的成熟。
人工提升橫紋肌肉瘤細胞中miR-29的水平會將癌細胞的增殖減半,，并促使它們開始成熟,，減慢了腫瘤生長。
科學家表示,，此次的研究與眾不同,，它闡明了小分子RNA自身如何被調(diào)控。Guttridge說：“研究表明miR-29,、肌肉發(fā)育和橫紋肌肉瘤之間存在聯(lián)系,。這一發(fā)現(xiàn)為我們提供了關于肌修復和發(fā)育以及橫紋肌肉瘤更深入的理解，有可能由此產(chǎn)生治療該病及其它肌肉疾病的新方法,。”（生物谷Bioon.com）
生物谷推薦原始出處：
Cancer Cell,，Volume 14, Issue 5, 369-381，Huating Wang,，Denis C. Guttridge
NF-κBYY1miR-29 Regulatory Circuitry in Skeletal Myogenesis and Rhabdomyosarcoma
Huating Wang1,Ramiro Garzon1,Hao Sun1,Katherine J. Ladner1,Ravi Singh2,Jason Dahlman1,Alfred Cheng1,4,Brett M. Hall2,Stephen J. Qualman2,Dawn S. Chandler2,Carlo M. Croce1,3andDenis C. Guttridge1,3,,
1 Human Cancer Genetics Program, Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, Columbus, OH 43210, USA
2 Department of Pediatrics, Nationwide Children's Hospital, The Ohio State University, Columbus, OH 43210, USA
3 The Arthur G. James Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA
4 Present address: Institute of Digestive Disease, Chinese University of Hong Kong, Hong Kong
Studies support the importance of microRNAs in physiological and pathological processes. Here we describe the regulation and function of miR-29 in myogenesis and rhabdomyosarcoma (RMS). Results demonstrate that in myoblasts, miR-29 is repressed by NF-κB acting through YY1 and the Polycomb group. During myogenesis, NF-κB and YY1 downregulation causes derepression of miR-29, which in turn accelerates differentiation by targeting its repressor YY1. However, in RMS cells and primary tumors that possess impaired differentiation, miR-29 is epigenetically silenced by an activated NF-κBYY1 pathway. Reconstitution of miR-29 in RMS in mice inhibits tumor growth and stimulates differentiation, suggesting that miR-29 acts as a tumor suppressor through its promyogenic function. Together, these results identify a NF-κBYY1miR-29 regulatory circuit whose disruption may contribute to RMS.
