BioMed Research International

Volume 2013 (2013), Article ID 514349, 2 pages

http://dx.doi.org/10.1155/2013/514349

Letter to the Editor

Tumor Growth Limiting Effects of Piceatannol

Shailendra Kapoor

74 Crossing Place, Mechanicsville, VA 23221, USA

Received 25 December 2012; Accepted 9 January 2013

Copyright © 2013 Shailendra Kapoor. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Kita et al. have provided interesting data in their recent article [1]. Piceatannol may attenuate tumor growth in a number of systemic malignancies besides hepatocellular carcinomas.

Similar effects are seen in prostatic malignancies. It mediates this role by augmenting tumoral apoptosis. There is increased cytochrome C release from the mitochondria. Piceatannol also causes downregulation of mTOR [2]. Piceatannol also has an inhibitory effect on IL-6/STAT3 signaling that further accentuates intratumoral apoptosis [3]. Besides these effects, piceatannol also decreases the release of VEGF. A simultaneous decrease in Akt and eIF-4E-BP1 accompanies the above changes. As a result, there is increased G1 phase arrest. Bik and Bok expression is also enhanced. “Urokinase-type plasminogen activator” secretion is also decreased [4]. The net result is that that tumor invasiveness is markedly attenuated. Tumor metastasis is markedly inhibited at the same time. Also, there is downregulation of PARP expression within the tumor cells. The levels of cleaved caspase-7 are augmented at the same time. At the same time Bcl-xL levels are downregulated while Bax levels are upregulated [5]. CDK4 and CDK2 activity is also attenuated.

Similarly, piceatannol attenuates tumor growth in breast carcinomas. It mediates this role by significantly inhibiting MMP-9. Similar inhibition of the NF-κB pathway accompanies the above changes [6]. Iκ-Bα phosphorylation is also attenuated resulting in decreased nuclear translocation of NF-κB. It also has an inhibitory effect on the PI3K/AKT pathway. Similar effects are seen in colorectal malignancies. Cyclin B1 expression is decreased secondary to piceatannol administration. Accumulation of cancerous cells in the S phase is accentuated. p27 (Kip1) levels are also downregulated [7]. Cyclin D1 expression is also decreased.

The above examples clearly indicate the significant tumor attenuating effects of piceatannol.

Conflict of Interests

There is no conflict of interests to declare.

References

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T. C. Hsieh, C. Y. Lin, H. Y. Lin, and J. M. Wu, “AKT/mTOR as novel targets of polyphenol piceatannol possibly contributing to inhibition of proliferation of cultured prostate cancer cells,” ISRN Urology, vol. 2012, Article ID 272697, 8 pages, 2012.

E. J. Kim, H. Park, S. Y. Park, J. G. Jun, and J. H. Y. Park, “The grape component piceatannol induces apoptosis in du145 human prostate cancer cells via the activation of extrinsic and intrinsic pathways,” Journal of Medicinal Food, vol. 12, no. 5, pp. 943–951, 2009.

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H. S. Ko, H. J. Lee, S. H. Kim, and E. O. Lee, “Piceatannol suppresses breast cancer cell invasion through the inhibition of MMP-9: involvement of PI3K/AKT and NF-kappaB pathways,” Journal of Agricultural and Food Chemistry, vol. 60, pp. 4083–4089, 2012.

F. Wolter, A. Clausnitzer, B. Akoglu, and J. Stein, “Piceatannol, a natural analog of resveratrol, inhibits progression through the s phase of the cell cycle in colorectal cancer cell lines,” Journal of Nutrition, vol. 132, no. 2, pp. 298–302, 2002.