Gamma-tocopherol inhibits human cancer cell cycle progression and cell proliferation by down-regulation of cyclins

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Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
06:00

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

Published on: May 14, 2016

René Gysin1, Angelo Azzi, Theresa Visarius

  • 1Institute of Biochemistry and Molecular Biology, University of Bern, Switzerland.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|October 9, 2002
PubMed

Insights

Gamma-tocopherol, a common dietary form of vitamin E, significantly inhibits cancer cell growth and DNA synthesis. This suggests a non-antioxidant mechanism for its anticancer effects, distinct from alpha-tocopherol.

Area of Science:

  • Oncology
  • Molecular Biology
  • Nutritional Science

Background:

  • Epidemiological studies suggest vitamin E possesses anticancer properties, but mechanistic insights are limited.
  • Vitamin E encompasses tocopherols (alpha-, beta-, gamma-, delta-) and tocotrienols.
  • Gamma-tocopherol is prevalent in the U.S. diet, while alpha-tocopherol dominates supplements.

Purpose of the Study:

  • To investigate the effects of gamma-tocopherol on cancer cell cycle progression and proliferation.
  • To compare the anticancer efficacy of gamma-tocopherol with alpha-tocopherol at physiologically relevant concentrations.
  • To elucidate the molecular mechanisms underlying gamma-tocopherol's antiproliferative effects.

Main Methods:

  • Cell cycle analysis using flow cytometry.
  • Measurement of DNA synthesis via 5-bromo-2'-deoxyuridine incorporation.
  • Western-blot analysis to assess cyclin D1 and cyclin E protein levels.

Main Results:

  • Gamma-tocopherol demonstrated greater growth inhibition in prostate carcinoma, colorectal adenocarcinoma, and osteosarcoma cells compared to alpha-tocopherol.
  • Flow cytometry revealed decreased S-phase progression in gamma-tocopherol treated DU-145 cells.
  • Reduced DNA synthesis and decreased levels of cyclin D1 and cyclin E were observed following gamma-tocopherol treatment.

Conclusions:

  • Gamma-tocopherol inhibits cancer cell cycle progression by downregulating cyclin D1 and cyclin E.
  • The potent antiproliferative and DNA synthesis inhibitory effects of gamma-tocopherol suggest a non-antioxidant mechanism.
  • Gamma-tocopherol warrants further investigation as a potential therapeutic agent against various cancers.

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