Up-regulation of microRNA-138 induce radiosensitization in lung cancer cells

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• 作者：Hui Yang (1)
  Yue Tang (2)
  Wei Guo (3)
  Yuwen Du (2)
  Yuanyuan Wang (2)
  Ping Li (4)
  Wenqiao Zang (2)
  Xiaojun Yin (5)
  Huaqi Wang (4)
  Heying Chu (4)
  Guojun Zhang (4)
  Guoqiang Zhao (2)
  
• 关键词：miR ; 138 ; SENP1 ; Radiosensitivity ; Lung cancer
• 刊名：Tumor Biology
• 出版年：2014
• 出版时间：July 2014
• 年：2014
• 卷：35
• 期：7
• 页码：6557-6565
• 全文大小：909 KB
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• 作者单位：Hui Yang (1)
  Yue Tang (2)
  Wei Guo (3)
  Yuwen Du (2)
  Yuanyuan Wang (2)
  Ping Li (4)
  Wenqiao Zang (2)
  Xiaojun Yin (5)
  Huaqi Wang (4)
  Heying Chu (4)
  Guojun Zhang (4)
  Guoqiang Zhao (2)
  
  1. Department of Nuclear Medicine, Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou, 450008, Henan, China
  2. College of Basic Medical Sciences, Zhengzhou University, No. 100 Kexue Road, Zhengzhou, 450001, Henan, China
  3. Henan Academy of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, 450052, Henan, China
  4. Department of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China
  5. Department of Emergency, The Third Affiliated Hospital of Henan University of TCM, Zhengzhou, 450003, Henan, China
  
• ISSN：1423-0380

文摘

Deregulation of microRNAs (miRNAs) is implicated in tumor progression. We attempt to identify the association between miR-138 and Sentrin/SUMO-specific protease 1 (SENP1) as a radiosensitization-related gene and characterize the biological function by which SENP1 was regulated by miR-138 to influence radiosensitization in lung cancer cells. In this study, we showed that miRNA-138 is reduced in both lung cancer clinical specimens and cell lines and is effective to inhibit SENP1 expression. Moreover, high levels of miR-138 are associated with lower levels of lung cancer cell proliferation and colony formation. Then, we investigated the underlying mechanisms responsible for the increase in the radiosensitivity of lung cancer cells when SENP1 is inhibited by miR-138. We further show that the increased radiosensitivity may be the result of an increased γ-H2AX expression, an increased rate of apoptosis, and changes in the cell cycle. In conclusion, our data demonstrate that the miR-138/SENP1 cascade is relative to radiosensitization in lung cancer cells and is a potential radiotherapy target.