PPM1D silencing by RNA interference inhibits the proliferation of lung cancer cells

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• 作者：Chen Zhang (1)
  Yuanzhuo Chen (1)
  Mingsong Wang (2)
  Xianzhen Chen (1)
  Yongxin Li (3)
  E Song (4)
  Xiaoqing Liu (1)
  Sekwon Kim (3)
  Hu Peng (1)
  
  1. Shanghai Tenth People鈥檚 Hospital ; Tongji University School of Medicine ; Shanghai ; 200072 ; China
  2. Department of Cardiothoracic Surgery ; Xinhua Hospital ; Shanghai Jiaotong University School of Medicine ; Shanghai ; 200092 ; China
  3. Department of Marine Bio Convergence Science ; Specialized Graduate School Science and Technology Convergence ; Pukyong National University ; Busan ; 608-737 ; Republic of Korea
  4. Lixiang Eye Hospital of Soochow University ; Suzhou ; Jiangsu ; 215000 ; China
  
• 关键词：PPM1D ; lung cancer ; shRNA ; cell proliferation ; cell cycle
• 刊名：World Journal of Surgical Oncology
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：12
• 期：1
• 全文大小：901 KB
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• 刊物主题：Surgical Oncology;
• 出版者：BioMed Central
• ISSN：1477-7819

文摘

Background PPM1D (protein phosphatase, Mg2+/Mn2+ dependent, 1D) has been reported to be involved in multiple human tumors. This study was designed to investigate the functional role of PPM1D in lung cancer cells. Methods Expression levels of PPM1D were analyzed in A549 and H1299 cells by real-time PCR and Western blotting. Lentivirus-mediated short hairpin RNA (shRNA) was used to knock down PPM1D expression in both cell lines. The effects of PPM1D on lung cancer cell growth were investigated by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide), colony formation and flow cytometry assays. Results Knockdown of PPM1D in lung cancer cells resulted in decreased cell proliferation and impaired colony formation ability. Moreover, flow cytometry analysis showed that knockdown of PPM1D arrested cell cycle at the G0/G1 phase. Furthermore, PPM1D silencing downregulated the expression of cyclin B1 in H1299 cells. Therefore, it is reasonable to speculate that the mechanisms by which PPM1D knockdown alleviates cell growth may be partly via the induction of cell cycle arrest due to the suppression of cyclin B1. Conclusions These results suggest that PPM1D silencing by RNA interference (RNAi) may be a potential therapeutic approach for the treatment of lung cancer.