MicroRNA-302b suppresses cell proliferation by targeting EGFR in human hepatocellular carcinoma SMMC-7721 cells

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• 作者：Lumin Wang (34)
  Jiayi Yao (34)
  Xin Shi (35)
  Lili Hu (34)
  Zongfang Li (36)
  Tusheng Song (34)
  Chen Huang (34) (37) (38)
  
• 关键词：miR ; 302b ; Hepatocellular carcinoma ; EGFR ; Proliferation ; Cell cycle
• 刊名：BMC Cancer
• 出版年：2013
• 出版时间：December 2013
• 年：2013
• 卷：13
• 期：1
• 全文大小：672 KB
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  41. The pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1471-2407/13/448/prepub
  
• 作者单位：Lumin Wang (34)
  Jiayi Yao (34)
  Xin Shi (35)
  Lili Hu (34)
  Zongfang Li (36)
  Tusheng Song (34)
  Chen Huang (34) (37) (38)
  
  34. Department of Genetics and Molecular Biology, Xi鈥檃n Jiaotong University Health Science Center, No.76 West Yanta Road, Xi鈥檃n, Shaanxi, 710061, P.R. China
  35. Xi鈥檃n IV People鈥檚 Hospital, Xi鈥檃n, Shaanxi, P.R. China
  36. Engineering Research Center of Biotherapy and Translational Medicine of Shaanxi Province, Xi鈥檃n, Shaanxi, P.R. China
  37. Key Laboratory of Environment and Genes Related to Diseases, Xi鈥檃n Jiaotong University Health Science Center, Xi鈥檃n, Shaanxi, China
  38. Cardiovascular Research Center, Xi鈥檃n Jiaotong University Health Science Center, Xi鈥檃n, Shaanxi, P.R. China
  
• ISSN：1471-2407

文摘

Background MicroRNAs are regulators that can play an essential role in tumorigenesis. Although miR-302 families have been suggested to be tumor repressors in human cancer, the mechanism by which they suppress tumor development remains to be defined. In this study, we discover that miR302b suppresses tumor proliferation may due to directly targeting EGFR in human hepatocellular carcinoma (HCC). Methods QRT-PCR was used to assess miR-302b and EGFR expression in 27 pairs of clinical hepatocellular carcinoma tissues and their corresponding adjacent nontumorous liver tissues. MTT, colony formation, immunofluorescence staining, and cell cycle assays were used to examine the tumor suppressor role of miR302b in cell proliferation. Luciferase assays were performed to assess the EGFR was a novel target of miR-302b. Western blot assay was used to validate the protein expression level. Results We demonstrated that miR-302b was frequently down-regulated, whereas EGFR was up-regulated in 27 pairs of clinical HCC and non-tumorous counterparts. The dual-luciferase reporter assays revealed that EGFR was a novel target of miR-302b. Re-expression of miR-302b resulted in the inhibition of proliferation in hepatocellular carcinoma SMMC-7721 cells. The silencing of EGFR by miR-302b or siEGFR led to down-regulation of proliferation-related proteins, such as AKT2, CCND1, and CDK2. Conclusion miR-302b suppresses HCC growth may due to targeting the EGFR/AKT2/CCND1 pathway.