Positive Health Online

Abstract

NESARETNAM and colleagues, Division of Cell and Molecular Biology, School of Animal and Microbial Sciences, The University of Reading, Whiteknights, UK sarnesar@porim.gov.my study the potential antiproliferative effects of tocotrienols, the vitamin E component in palm oil, upon human breast cancer cell growth .

Background

Methodology

Both oestrogen-responsive (ER+) MCF7 and oestrogen- unresponsive (ER-) MDA-MB-231 human breast cancer cells were used in this study. The effects of the tocotrienol rich fraction (TRF) of palm oil were compared with those of alpha-tocopherol (alphaT) .Results: TRF inhibited growth of MCF7 cells (ER+) both in the presence and absence of oestradiol ; the dose-response was nonlinear, and complete suppression of growth was achieved at 8 microgram/ml. MDA-MB-231 (ER-) cells were also inhibited by TRF; there was a linear dose-response and complete growth suppression was achieved with 20 microgram/ml. Fractionation of the TRF into individual tocotrienols revealed that all the fractions inhibited the growth of both ER+ and ER- cells, and of ER+ cells both in the presence and absence of oestradiol . The most highly inhibitory were the gamma- and delta-fractions; complete inhibition of MCF7 cell growth was achieved at 6 micrograms/ml of gamma-tocotrienol/delta-tocotrienol (gammaT3/deltaT3) in the absence of oestradiol and 10 micrograms/ml of deltaT3 in the presence of oestradiol. Complete suppression of growth of MDA-MB-231 (ER-) cells was not achieved even at concentrations of 10 micrograms/ml deltaT3. In contrast to the inhibitory effects of tocotrienols, alphaT had no inhibitory effect upon MCF7 nor on MDA-MB-231 cell growth either in the presence or absence of oestradiol .

Results

Conclusion

These data confirm results from other studies using other sublines of human breast cancer cells and demonstrate that tocotrienols exert direct inhibitory effects upon breast cancer cell growth . Studies of the effects of TRF upon oestrogen-regulated pS2 gene expression in MCF7 showed that tocotrienols do not act via an oestrogen receptor-mediated pathway and must therefore act differently from oestrogen antagonists. Also, tocotrienols did not increase levels of growth-inhibitory insulin-like growth factor binding proteins (IGFBP) in MCF7 cells, implying a different mechanism from the one proposed for retinoic acid inhibition of oestrogen-responsive breast cancer cell growth. Clinical Implications: The inhibition of breast cancer cell growth by tocotrienols may have important clinical implications not only because tocotrienols inhibit the growth of both ER+ and ER- cells types, but also because ER+ cells could be growth-inhibited in the presence as well as in the absence of oestradiol. Future clinical applications of TRF may arise from potential growth suppression of ER+ breast cancer cells which are resistant to growth inhibition by antioestrogens and retinoic acid.

References

Nesaretnam K ete al Tocotrienols inhibit the growth of human breast cancer cells irrespective of estrogen receptor status Lipids 33(50: 461-9 May 1998

Comment

The above studies demonstrate the real progress being made at molecular and biochemical levels to elucidate the roles of foods and dietary supplements in the treatment and prevention of cancer. The denial by large swathes of the medical profession of the role of dietary agents in cancer treatment and prevention, in light of this quality of published research in the public domain is either a testament to their ignorance of the research, or else a deliberate conspiracy to ignore the evidence.