Down-regulation of miR-150 induces cell proliferation inhibition and apoptosis in non-small-cell lung cancer by targeting BAK1 in vitro

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• 作者：Xiao-yan Gu (1)
  Jun Wang (2)
  Yi-zhou Luo (3)
  Qiang Du (4)
  Ruo-ran Li (5)
  Hui Shi (6)
  Tian-pei Yu (1)
  
• 关键词：miR ; 150 ; Proliferation ; Apoptosis ; Non ; small ; cell lung cancer
• 刊名：Tumor Biology
• 出版年：2014
• 出版时间：June 2014
• 年：2014
• 卷：35
• 期：6
• 页码：5287-5293
• 全文大小：
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• 作者单位：Xiao-yan Gu (1)
  Jun Wang (2)
  Yi-zhou Luo (3)
  Qiang Du (4)
  Ruo-ran Li (5)
  Hui Shi (6)
  Tian-pei Yu (1)
  
  1. Department of Rehabilitation, The 454th Hospital of Chinese PLA, Nanjing, Jiangsu, 210002, China
  2. Department of Respiratory, Suzhou Kowloon Hospital affiliated with Shanghai Jiao Tong University School of Medicine, Suzhou, 215021, China
  3. Department of Oncology, The 454th Hospital of Chinese PLA, Nanjing, Jiangsu, 210002, China
  4. Department of Respiratory Medicine, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, 210011, China
  5. Department of Respiratory Medicine, Xuzhou Central Hospital, Xuzhou, Jiangsu, 221009, China
  6. Department of Gastroenterology, Jinling Hospital, Nanjing, 210002, China
  
• ISSN：1423-0380

文摘

Non-small-cell lung cancer (NSCLC) is one of the most common causes of cancer-related death. Our investigations show that miR-150 is a typical microRNA that is overexpressed in human NSCLC. We characterized the effects of miR-150 overexpression in NSCLC cells and found that down-regulation of miR-150 expression inhibited cell proliferation and induced cell apoptosis in vitro; additionally, up-regulation of miR-150 levels had the opposite effect on tumor growth and progression. Furthermore, we found that the mechanism of the miR-150 effects on NSCLC cells was associated with alterations in the expression of human BRI1-associated receptor kinase 1 (BAK1). miR-150 may function as an oncogene in NSCLC cells by directly targeting BAK1. Thus, these data highlight a novel molecular interaction between miR-150 and BAK1 and provide a novel strategy for NSCLC therapy via the down-regulation of miR-150 expression.