Lycopene Interferes with Cell Progression and IGF-1 Signaling in Mammary Cancer Cells

The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 6 No. 1 • February 2003

Lycopene Interferes with Cell Progression and IGF-1 Signaling in Mammary Cancer Cells

There is evidence that IGF-1 (insulinlike growth factor 1) signaling may play a role in certain cancers (such as prostate, breast, lung, and colorectal in women) by acting as a mitogen (a substance that increases cell proliferation) and inhibiting apoptosis (programmed cell death). In observational studies, higher levels of IGF-1 are associated with higher risks of these and possibly other cancers.1 Hence, interfering with IGF-1 signaling, especially if such interference can be localized to high-risk tissues sensitive to its mitogenic effects,2 would be very desirable in terms of reducing cancer risk.

A recent paper8 reports that, in mammary cancer cells, growth stimulation by IGF-1 was markedly reduced by lycopene treatment. The researchers note that these effects were not associated with changes in the number or affinity of IGF-1 receptors, but were a result of an increase in membrane-associated IGF-binding proteins, which were shown previously to negatively regulate IGF-1 receptor activation in different cancer cells. Moreover, they report that lycopene inhibited basal and IGF-induced thymidine incorporation into DNA (as a measure of growth) and slowed cell cycle progression, while not causing cell death. These same authors had previously reported that lycopene inhibited mammary, endometrial, and lung cancer cell growth in a dose-dependent manner; the concentration causing 50% inhibition was approximately 2 microM. The latter inhibition was detected after 24 hours of incubation and was maintained for at least three days.


  1. See, e.g., a review by Yu and Rohan, Role of the insulin-like growth factor family in cancer development and progression. J Natl Cancer Inst 92(18):1472-89 (2000).
  2. On the other hand, IGF-1 has shown protective effects in the pathogenesis of diabetic angiopathy,3 in accelerating muscle and motor neuron regeneration,4 in enhancing DNA accretion and growth in skeletal muscle,5 and possibly in enhancing the removal of amyloid-beta from the brain.6 Recently, transgenic mice (which had one gene for the IGF-1 receptor knocked out, while the other gene was normal) had greater resistance to oxidative stress and lived an average of 26% longer than their wild-type littermates (the 16% increase in lifespan for the male mice was not statistically significant, however; the male mice, but not females, also had abnormal blood glucose regulation).7 Hence, the overall picture for the risk/benefit of IGF-1 is decidedly complex.
  3. Janssen and Lamberts. Circulating IGF-1 and its protective role in the pathogenesis of diabetic angiopathy. Clin Endocrinol 52:1-9 (2000).
  4. Rabinovsky et al. Targeted expression of IGF-1 transgene to skeletal muscle accelerates muscle and motor neuron regeneration. FASEB J (Nov. 1, 2002).
  5. Fiorotto et al. Persistent IGF-1 overexpression in skeletal muscle transiently enhances DNA accretion and growth. FASEB J (Nov. 15, 2002).
  6. Carro et al. Serum insulin-like growth factor 1 regulates brain amyloid-beta levels. Nature Med 8(12):1390-7 (2002). See last issue of this newsletter for discussion.
  7. Holzenberger et al. IGF-1 receptor regulates lifespan and resistance to oxidative stress in mice. Nature 421:182-7 (2003).
  8. Karas et al. Lycopene interferes with cell cycle progression and insulin-like growth factor 1 signaling in mammary cancer cells. Nutr Cancer 36(1):101-111 (2000).

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