Small nucleolar RNA 78 promotes the tumorigenesis in non-small cell lung cancer

Journal of Experimental & Clinical Cancer Research

Gang Chen²  Bo Su¹  Jianfang Xu³  Li Wang³  Ling Zhang³  Liang Tang¹  Jiying Wang³  Jie Luo³  Jian Ni³  Jie Zhang¹  Di Zheng³ 

[1] Central Lab, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China;Department of Pathology, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai 200032, People’s Republic of China;Department of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, 507 Zhengmin Road, Shanghai 200433, People’s Republic of China

关键词: Cancer stem-like cell;    Epithelial-mesenchymal-transition;    SNORD78;    Small nucleolar RNA;    Non-small cell lung cancer;   

Others  :  1220699
DOI  :  10.1186/s13046-015-0170-5

 received in 2015-02-12, accepted in 2015-05-08,  发布年份 2015

【 摘 要 】

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.

【 授权许可】

   
2015 Zheng et al.

【 图 表 】

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