Oncogene文章：microRNA-133b是宮頸癌發生與發展的關鍵因素
 

　　宮頸癌（cervical carcinoma）是女性第二大惡性腫瘤，并且在年輕女性中發病率高。2002年全世界的新發病例為50萬人，死亡病例為27萬人。根據中國疾病預防與控制中心公布的數據，我國每年宮頸癌新發病例為13.15 萬人，約占世界總數的26%，死亡病例為5.3 萬人，約占世界總數的20%。因此，我國的宮頸癌防治形勢非常嚴峻。
 
　　在99.8%的宮頸癌患者中均可檢測到HPV感染。但單獨的HPV 感染不足以引起宮頸癌，細胞本身必須發生相應的變化，才能最終引起宮頸癌。清華大學的程京教授與新疆醫科大學第一附屬醫院的溫浩教授合作，利用生物芯片平臺研究了宮頸癌組織中microRNA的表達變化，發現了20種microRNA在宮頸癌的發生和發展過程中表達量發生了改變。其中microRNA-133b在從宮頸上皮內瘤樣病變到侵潤癌的發展過程中，表達量逐步升高。功能學實驗結果表明，這一microRNA具有促進宮頸癌發生和發展的作用。該microRNA有可能作為臨床早期診斷的新型宮頸癌標志物。
　　上述研究成果已申請專利，研究論文已在Oncogene雜志網站在線發表。其中的博奧生物晶芯^®哺乳動物miRNA芯片服務與Real time RT-PCR服務在博奧生物有限公司完成。

原文摘要：

　　MicroRNA-133b is a key promoter of cervical carcinoma development through the activation of the ERK and AKT1 pathways
 
　　We report that elevated microRNA-133b (miR-133b) acts as an oncogene in human cervical carcinoma to promote tumorigenesis and metastasis. In situ hybridization confirmed that miR-133b is localized in proliferating human cervical carcinoma cells with levels progressively elevating throughout advancing stages. Cellular studies showed that miR-133b enhances cell proliferation and colony formation by targeting mammalian sterile 20-like kinase 2 (MST2), cell division control protein 42 homolog (CDC42) and ras homolog gene family member A (RHOA), which subsequently results in activation of the tumorigenic protein kinase B alpha (AKT1) and mitogenactivated protein kinase (ERK1 and ERK2, here abbreviated as ERK) signaling pathways. Mouse experiments revealed that upregulation of miR-133b in cervical carcinoma cells strongly promotes both in vivo tumorigenesis and independent metastasis to the mouse lung. The data indicates that upregulation of miR-133b shortens the latency of cervical carcinoma. Together, these findings suggest that miR-133b could be a potent marker for the early onset of cervical carcinoma.
 
原文出處：http://www.nature.com/onc/journal/vaop/ncurrent/abs/onc2011561a.html