Tumor invasion and metastasis regulated by microRNA-184 and microRNA-574-5p in small-cell lung cancer

被引:52
作者
Zhou, Rui [1 ]
Zhou, Xiaoshu [1 ]
Yin, Zhongyuan [1 ]
Guo, Jing [2 ]
Hu, Ting [1 ]
Jiang, Shun [3 ]
Liu, Li [1 ]
Dong, Xiaorong [1 ]
Zhang, Sheng [1 ]
Wu, Gang [1 ]
机构
[1] Huazhong Univ Sci & Technol, Tongji Med Coll, Union Hosp, Ctr Canc, Wuhan 430074, Peoples R China
[2] Qingdao Univ, Affiliated Hosp, Dept Oncol, Qingdao 266071, Peoples R China
[3] Cent S Univ, Xiangya Hosp 2, Dept Oncol, Changsha, Hunan, Peoples R China
基金
中国国家自然科学基金;
关键词
miR-184; miR-574-5p; metastasis; prognosis; SCLC; PROTEIN-TYROSINE-PHOSPHATASE; C-MYC; MATURE MIR-184; BETA-CATENIN; EXPRESSION; SURVIVAL; GROWTH; BIOMARKERS; CARCINOMA; DIAGNOSIS;
D O I
10.18632/oncotarget.6338
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Small-cell lung cancer (SCLC) is a highly aggressive neuroendocrine tumor that has an extremely poor clinical prognosis. Metastasis is the key event in SCLC progression, but its mechanism has not been fully elucidated. MicroRNAs (miRNAs) have been proven to participate in cancer processes, but their function in SCLC has not been thoroughly studied either. Here, we performed microarray and quantitative real-time PCR (qRT-PCR) analyses to identify the miRNAs associated with metastasis and prognosis in SCLC as well as the correlation between serum and tissue. We also explored these miRNAs' promising molecular mechanisms by 3'UTR reporter assay and immunoblotting. We showed thatmiR-184 significantly attenuated the metastasis of SCLC, whereas miR-574-5p enhanced it. Both miRNAs were found to participate in beta-catenin signaling by suppressing protein tyrosine phosphatase receptor type U (PTPRU) orendothelial PAS domain protein 1 (EPAS1). Furthermore, miR-574-5p was verified as an independent prognostic risk factor for SCLC. Taken together, our findings providea comprehensive analysis of the miRNA expression pattern in SCLC and indicate that miRNAs may serve as potential therapeutic and prognostic predictors in SCLC.
引用
收藏
页码:44609 / 44622
页数:14
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