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Inhibition of cell transformation by resveratrol and its derivatives: Differential effects and mechanisms involved

  • Qing Bai She
  • , Wei Ya Ma
  • , Mingfu Wang
  • , Akira Kaji
  • , Chi Tang Ho
  • , Zigang Dong

Research output: Contribution to journalArticlepeer-review

56 Scopus citations

Abstract

Resveratrol, a constituent of grapes and other foods, has been reported to be a potential cancer chemopreventive agent. Our previous study showed that the antitumor activity of resveratrol occurs through mitogen-activated protein kinases-mediated p53 activation and induction of apoptosis. To develop more effective agents with fewer side effects for the chemoprevention of cancer, we investigated the effect of resveratrol and its structurally related derivatives on epidermal growth factor (EGF)-induced cell transformation. Our results provided the first evidence that one of the resveratrol derivatives exerted a more potent inhibitory effect than resveratrol on EGF-induced cell transformation, but had less cytotoxic effects on normal nontransformed cells. Compared to resveratrol, this compound also caused cell cycle arrest in the G1 phase, but did not induce p53 activation and apoptosis. Furthermore, this compound, but not resveratrol, markedly inhibited EGF-induced phosphatidylinositol-3 kinase (PI-3K) and Akt activation. Collectively, these data suggested that the higher antitumor effect of the compound compared to resveratrol, may act through a different mechanism by mainly targeting PI-3K/Akt signaling pathways.

Original languageEnglish
Pages (from-to)2143-2150
Number of pages8
JournalOncogene
Volume22
Issue number14
DOIs
StatePublished - Apr 10 2003

Bibliographical note

Funding Information:
We thank Dr Ann M Bode for critical reading of the manuscript, Patricia Schmid for analysis of cell cycle and apoptosis, Qing Ye for help with some experiments and Andria Hansen for secretarial assistance. This work was supported in part by The Hormel Foundation, American Institutes for Cancer Research Grant 99A062, and National Institutes of Health Grants CA77646 and CA81064.

Funding

We thank Dr Ann M Bode for critical reading of the manuscript, Patricia Schmid for analysis of cell cycle and apoptosis, Qing Ye for help with some experiments and Andria Hansen for secretarial assistance. This work was supported in part by The Hormel Foundation, American Institutes for Cancer Research Grant 99A062, and National Institutes of Health Grants CA77646 and CA81064.

FundersFunder number
National Institutes of Health (NIH)CA77646
National Childhood Cancer Registry – National Cancer InstituteR37CA081064
American Institute for Cancer Research99A062
Hormel Foundation

    UN SDGs

    This output contributes to the following UN Sustainable Development Goals (SDGs)

    1. SDG 3 - Good Health and Well-being
      SDG 3 Good Health and Well-being

    Keywords

    • Cell transformation
    • Chemoprevention
    • PI-3K/Akt
    • Resveratrol
    • Resveratrol derivatives
    • p53

    ASJC Scopus subject areas

    • Molecular Biology
    • Genetics
    • Cancer Research

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