Korean Journal of Plant Resources (한국자원식물학회지)

The Plant Resources Society of Korea (한국자원식물학회)
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Anticancer Activity of the Branch Extracts from Vaccinium oldhamii through Cyclin D1 Proteasomal Degradation in Human Cancer Cells

  • Park, Su Bin (Department of Medicinal Plant Resources, Andong National University) ;
  • Kim, Ha Na (Department of Medicinal Plant Resources, Andong National University) ;
  • Park, Gwang Hun (Forest Medicinal Resources Research Center, National Institute of Forest Science) ;
  • Son, Ho-Jun (Forest Medicinal Resources Research Center, National Institute of Forest Science) ;
  • Eo, Hyun Ji (Forest Medicinal Resources Research Center, National Institute of Forest Science) ;
  • Song, Jeong Ho (Forest Medicinal Resources Research Center, National Institute of Forest Science) ;
  • Song, Hun Min (Baekdudaegan National Arboretum) ;
  • Park, Ji Ae (Baekdudaegan National Arboretum) ;
  • Jeong, Jin Boo (Department of Medicinal Plant Resources, Andong National University)
  • Received : 2018.05.29
  • Accepted : 2018.06.12
  • Published : 2018.06.30
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Abstract

In this study, we investigated the effect of the extracts from Vaccinium oldhamii on cell proliferation and the regulatory mechanisms of cyclin D1 protein level in human cancer cells. The branch extracts from Vaccinium oldhamii (VOB) showed higher inhibitor effect against the cell growth than leave extracts (VOL) and fruit extracts (VOF) in human colorectal cancer, breast cancer, prostate cancer, non-small lung cancer, pancreatic cancer and liver cancer cells. In addition, VOB decreased cyclin D1 level at both protein and mRNA level. MG132 treatment attenuated VOB-mediated cyclin D1 downregulation. A point mutation of threonine-286 to alanine attenuated cyclin D1 degradation by VOB. In addition, the inhibition of nuclear export by leptomycin B (LMB) attenuated cyclin D1 degradation by VOB. But, the treatment of PD98059 (ERK1/2 inhibitor), SB203580 (p38 inhibitor), SP600125 (JNK inhibitor), LiCl ($GSK3{\beta}$ inhibitor), LY294002 (PI3K inhibitor) or BAY 11-7082 ($I{\kappa}K$ inhibitor) did not affect VOB-induced cyclin D1 degradation. In conclusion, VOB induced cyclin D1 degradation through redistribution of cyclin D1 from the nucleus to cytoplasm via T286 phosphorylation of cyclin D1, which resulted in the inhibition of cancer cell proliferation.

Keywords

References

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