miR-145 functions as tumor suppressor and targets two oncogenes, ANGPT2 and NEDD9, in renal cell carcinoma

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• 作者：Ruijing Lu (1) (2)
  Ziliang Ji (2) (3)
  Xiaoqing Li (1) (2)
  Qingna Zhai (1) (2)
  Chunjuan Zhao (1) (2)
  Zhimao Jiang (3)
  Shiqiang Zhang (3)
  Liping Nie (1)
  Zhendong Yu (4)
  
• 关键词：miR ; 145 ; Tumor suppressor ; Renal cell carcinoma ; ANGPT2 ; NEDD9
• 刊名：Journal of Cancer Research and Clinical Oncology
• 出版年：2014
• 出版时间：March 2014
• 年：2014
• 卷：140
• 期：3
• 页码：387-397
• 全文大小：1,244 KB
• 作者单位：Ruijing Lu (1) (2)
  Ziliang Ji (2) (3)
  Xiaoqing Li (1) (2)
  Qingna Zhai (1) (2)
  Chunjuan Zhao (1) (2)
  Zhimao Jiang (3)
  Shiqiang Zhang (3)
  Liping Nie (1)
  Zhendong Yu (4)
  
  1. Department of Clinical Laboratory, Peking University Shenzhen Hospital, Shenzhen, 518036, China
  2. Shantou University Medical College, Shantou, 515041, China
  3. Guangdong and Shenzhen Key Laboratory of Male Reproductive Medicine and Genetics, Shenzhen PKU-HKUST Medical Center, Institute of Urology, Peking University Shenzhen Hospital, Shenzhen, 518036, China
  4. Central Laboratory, Peking University Shenzhen Hospital, Shenzhen, 518036, China
  
• ISSN：1432-1335

文摘

Purpose Abnormal expression of miRNAs is closely related to a variety of human cancers. The purpose of this study is to identify new tumor suppressor miRNA and elucidate its physiological function and mechanism in renal cell carcinoma (RCC). Methods The expression of miR-145 in 45 RCC and adjacent normal tissues was performed by quantitative RT-PCR. Cell proliferation, migration, invasion, apoptosis and cycle assays were carried out for functional analysis after miR-145 transfection. Two target genes of miR-145 were identified by luciferase reporter assay. The altered expression of 84 epithelial to mesenchymal transition (EMT)-related genes after miR-145 transfection was detected by RT2 Profiler EMT PCR array. Results The expression of miR-145 was downregulated in RCC compared to their normal adjacent tissues. Restoring miR-145 expression in RCC cell lines dramatically suppressed cell proliferation, migration and invasion, and induced cell apoptosis and G2-phase arrest. We further validated those miR-145 targets two oncogenes, ANGPT2 and NEDD9 in RCC. In addition, miR-145 was found to regulate numerous genes involved in the EMT. Conclusions These findings demonstrate that miR-145 functions as tumor suppressor in RCC, suggesting that miR-145 may be a potential therapeutic target for RCC.