4.6 Article

Mechanism of Pterostilbene-Induced Cell Death in HT-29 Colon Cancer Cells

Journal

MOLECULES
Volume 27, Issue 2, Pages -

Publisher

MDPI
DOI: 10.3390/molecules27020369

Keywords

pterostilbene apoptosis; autophagy; AKT; STAT3; colon cancer

Funding

  1. Medical University of Silesia (Katowice, Poland) [KNW-1-036/K/9/I]

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Pterostilbene, a dietary phytochemical, has been found to possess antioxidant and anti-inflammatory properties and shows potential as an anticancer agent. This study aimed to investigate the anticancer activity of pterostilbene against HT-29 human colon cancer cells and revealed that it inhibits cell proliferation and induces cell death. The effects of pterostilbene on cell cycle progression and signaling pathways were also evaluated. The down-regulation of STAT3 and AKT kinase pathways was found to mediate the anticancer activity of pterostilbene. These findings suggest that pterostilbene could be a promising therapeutic option for colon cancer in the future.
Pterostilbene is a dietary phytochemical that has been found to possess several biological activities, such as antioxidant and anti-inflammatory. Recent studies have shown that it exhibits the hallmark characteristics of an anticancer agent. The aim of the study was to investigate the anticancer activity of pterostilbene against HT-29 human colon cancer cells, focusing on its influence on cell growth, differentiation, and the ability of this stilbene to induce cell death. To clarify the mechanism of pterostilbene activity against colon cancer cells, changes in the expression of several genes and proteins that are directly related to cell proliferation, signal transduction pathways, apoptosis, and autophagy were also evaluated. Cell growth and proliferation of cells exposed to pterostilbene (5-100 mu M) were determined by SRB and BRDU assays. Flow cytometric analyses were used for cell cycle progression. Further molecular investigations were performed using quantitative real-time RT-PCR. The expression of the signaling proteins studied was determined by the ELISA method. The results revealed that pterostilbene inhibited proliferation and induced the death of HT-29 colon cancer cells. Pterostilbene, depending on concentration, caused inhibition of proliferation, G1 cell arrest, and/or triggered apoptosis in HT-29 cells. These effects were mediated by the down-regulation of the STAT3 and AKT kinase pathways. It may be concluded that pterostilbene could be considered as a potential therapeutic option in the treatment of colon cancer in the future.

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