小核仁RNA 78促进非小细胞肺癌的肿瘤发生。
Small nucleolar RNA 78 promotes the tumorigenesis in non-small cell lung cancer.
作者信息
Zheng Di, Zhang Jie, Ni Jian, Luo Jie, Wang Jiying, Tang Liang, Zhang Ling, Wang Li, Xu Jianfang, Su Bo, Chen Gang
机构信息
Department of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, 507 Zhengmin Road, Shanghai, 200433, People's Republic of China.
Central Lab, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
出版信息
J Exp Clin Cancer Res. 2015 May 15;34(1):49. doi: 10.1186/s13046-015-0170-5.
BACKGROUND
Accumulating evidence suggests that dysregulated snoRNA may play a role in the development of malignancy. In the present study, we investigated the role of SNORD78 in the tumorigenesis of non-small cell lung cancer (NSCLC).
METHODS
We determined the expression level of SNORD78 in NSCLC tissues with quantitative real-time PCR and then studied its clinical significance. We explored the biological significance of SNORD78 with gain-and-loss-of-function analyses both in vitro and in vivo.
RESULTS
A great upregulation of SNORD78 was observed in cancer tissues compared to their adjacent normal tissues. Meanwhile, patients with high SNORD78 expression have significantly poorer prognosis than those with low expression. Inhibition of SNORD78 suppressed the proliferation of NSCLC cells via inducing G0/G1 cell cycle arrest and apoptosis while SNORD78 overexpression promoted the cell proliferation. SNORD78 promoted invasion of NSCLC cells via inducing epithelial-mesenchymal-transition (EMT). SNORD78 was also obviously upregulated in cancer stem-like cells and is required for the self-renewal of NSCLC. The oncogenic activity of SNORD78 was also confirmed with in vivo data.
CONCLUSION
Our study identified that SNORD78 may be a potential therapeutic target for NSCLC.
背景
越来越多的证据表明，失调的小核仁RNA（snoRNA）可能在恶性肿瘤的发生发展中起作用。在本研究中，我们调查了小核仁RNA 78（SNORD78）在非小细胞肺癌（NSCLC）肿瘤发生中的作用。
方法
我们通过定量实时PCR测定NSCLC组织中SNORD78的表达水平，然后研究其临床意义。我们在体外和体内通过功能获得和功能丧失分析探讨了SNORD78的生物学意义。
结果
与相邻正常组织相比，癌组织中观察到SNORD78显著上调。同时，SNORD78高表达患者的预后明显比低表达患者差。抑制SNORD78通过诱导G0/G1期细胞周期阻滞和凋亡抑制NSCLC细胞的增殖，而SNORD78过表达促进细胞增殖。SNORD78通过诱导上皮-间质转化（EMT）促进NSCLC细胞的侵袭。SNORD78在癌干细胞样细胞中也明显上调，并且是NSCLC自我更新所必需的。体内数据也证实了SNORD78的致癌活性。
结论
我们的研究表明，SNORD78可能是NSCLC的一个潜在治疗靶点。
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