Oncology Reports

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Resveratrol epigenetically regulates the expression of zinc finger protein 36 in non-small cell lung cancer cell lines

  • Ahmad Fudhaili (Department of Anatomy and Convergence Medical Science, Institute of Health Sciences, College of Medicine, Gyeongsang National University) ;
  • Nal Ae Yoon (Department of Anatomy and Convergence Medical Science, Institute of Health Sciences, College of Medicine, Gyeongsang National University) ;
  • Seokmin Kang (Department of Anatomy and Convergence Medical Science, Institute of Health Sciences, College of Medicine, Gyeongsang National University) ;
  • Jinhyun Ryu (Department of Anatomy and Convergence Medical Science, Institute of Health Sciences, College of Medicine, Gyeongsang National University) ;
  • Joo Yeon Jeong (Department of Anatomy and Convergence Medical Science, Institute of Health Sciences, College of Medicine, Gyeongsang National University) ;
  • Dong Hoon Lee (Department of Anatomy and Convergence Medical Science, Institute of Health Sciences, College of Medicine, Gyeongsang National University) ;
  • Sang Soo Kang (Department of Anatomy and Convergence Medical Science, Institute of Health Sciences, College of Medicine, Gyeongsang National University)
  • Published : 20190200
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Abstract

Zinc finger protein 36 (ZFP36) is an AU-rich element protein that binds to 3'-untranslated regions and promotes the decay of target mRNAs. Downregulation of ZFP36 expression in turn results in stabilization of target mRNAs. A recent study indicated that downregulation of ZFP36 expression in human liver cancer is caused by epigenetic mechanisms. The purpose of the present study was to investigate the potential of resveratrol (Res) to induce ZFP36 expression. Promoter methylation was analyzed using methylation-sensitive restriction analysis. It was determined that Res treatment increased ZFP36 expression and decreased the mRNA levels of ZFP36 target genes in A549 lung cancer cells. Additionally, Res suppressed the expression of DNA (cytosine-5)-methyltransferase 1 and induced demethylation of the ZFP36 promoter. Collectively, the present results demonstrated that Res has anticancer activity through its epigenetic regulation of ZFP36 in non-small cell lung cancer.

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Acknowledgement

The authors would like to thank Dr Jeong Woo Park (University of Ulsan, Ulsan, Korea) for their supports of ZFP36 associated materials.