近日,，中國(guó)科技大學(xué)吳緬教授研究組與澳大利亞紐卡斯?fàn)柎髮W(xué)張旭東教授合作,，發(fā)現(xiàn)一種微小RNA149*分子參與了黑色素腫瘤的發(fā)生和發(fā)展，并揭示該小分子促進(jìn)黑色素瘤發(fā)生的新機(jī)制,。相關(guān)研究成果近期發(fā)表在國(guó)際著名學(xué)術(shù)期刊《美國(guó)科學(xué)院院刊》（PNAS）上,。這項(xiàng)研究成果，有望給黑色素瘤的診斷和治療帶來(lái)新的希望,。
黑色素瘤俗稱皮膚癌,，是一種危害性很大、發(fā)病率很高的惡性腫瘤,。吳緬等研究人員通過(guò)對(duì)60位黑色素瘤臨床病人的病例樣本的分析研究,，證實(shí)了RNA149*分子的含量較健康人正常組織呈顯著上升，這意味著該小分子可以作為黑色素瘤臨床診斷的依據(jù),。另外,，小鼠實(shí)驗(yàn)表明，降低該小分子含量可以明顯抑制黑色素瘤的生長(zhǎng),，這為治療黑色素瘤提供了一個(gè)潛在靶位,，用于臨床藥物的研發(fā)。專家稱,，這一研究成果將有可能用于改善黑色素瘤的診斷和治療,。（生物谷Bioon.com）
doi:10.1073/pnas.1019312108
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MicroRNA-149*, a p53-responsive microRNA, functions as an oncogenic regulator in human melanoma
Lei Jin, Wang Lai Hu, Chen Chen Jiang, Jia Xu Wang, Chuan Chun Han, Ping Chu, Lin Jie Zhang, Rick F. Thorne, James Wilmott, Richard A. Scolyer, Peter Hersey, Xu Dong Zhang, and Mian Wu
The tumor suppressor p53 is activated in response to cellular stress to prevent malignant transformation by activation of the DNA repair machinery to preserve the cell, or by induction of apoptosis to eliminate the cell should the damage prove irrevocable. The gene encoding p53 frequently undergoes inactivating mutations in many human cancers, but WT p53 is often expressed at high levels in melanoma, which, as judged from the malignant nature of the disease, fails to act as an effective tumor suppressor. Here we show that p53 directly up-regulates microRNA-149* (miR-149*) that in turn targets glycogen synthase kinase-3α, resulting in increased expression of Mcl-1 and resistance to apoptosis in melanoma cells. Although deficiency in miR-149* undermined survival of melanoma cells and inhibited melanoma growth in a mouse xenograft model, elevated expression of miR-149* was found in fresh human metastatic melanoma isolates, which was associated with decreased glycogen synthase kinase-3α and increased Mcl-1. These results reveal a p53-dependent, miR-149*–mediated pathway that contributes to survival of melanoma cells, provides a rational explanation for the ineffectiveness of p53 to suppress melanoma, and identifies the expression of miR-149* as a mechanism involved in the increased expression of Mcl-1 in melanoma cells.
