Pro‑apoptotic and migration‑suppressing potential of EGCG, and the involvement of AMPK in the p53‑mediated modulation of VEGF and MMP‑9 expression

Park,Song  Yi; Jung,Chang   Hee; Song,Bokyung; Park,Ock   Jin; Kim,Young‑Min

doi:10.3892/ol.2013.1533

Pro‑apoptotic and migration‑suppressing potential of EGCG, and the involvement of AMPK in the p53‑mediated modulation of VEGF and MMP‑9 expression

Authors:
- Song Yi Park
- Chang Hee Jung
- Bokyung Song
- Ock Jin Park
- Young‑Min Kim
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Affiliations: Department of Biological Sciences and Biotechnology, Hannam University Daedeok Valley Campus, Yuseong‑gu, Daejeon 305‑811, Republic of Korea, Department of Food and Nutrition, Hannam University Daedeok Valley Campus, Yuseong‑gu, Daejeon 305‑811, Republic of Korea
Published online on: August 19, 2013 https://doi.org/10.3892/ol.2013.1533
Pages: 1346-1350

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Abstract

The present study investigated the regulatory mechanisms by which epigallocatechin‑3‑gallate (EGCG) exerts vascular endothelial growth factor (VEGF)‑, p53‑ and AMP‑activated protein kinase (AMPK)‑associated pro‑apoptotic and migration‑suppressing effects on colon cancer cells. EGCG decreased the expression levels of VEGF and matrix metalloproteinase (MMP)‑9. EGCG treatment induced apoptosis in the presence of wild‑type and mutant p53, indicating that a p53‑independent pathway may contribute to EGCG‑induced apoptosis in these cells. EGCG showed migration‑suppressing effects, suggesting that this activity may also have p53‑dependent and ‑independent components. The interaction between p53 and VEGF in the EGCG‑treated cells was investigated using pifithrin‑α. Notably, the suppression of p53 activity blocked the ability of EGCG to inhibit VEGF and MMP‑9 in the cells expressing wild‑type p53, but not mutant p53, indicating that the effects of EGCG on VEGF may be p53‑dependent or ‑independent. Finally, although AMPK and VEGF did not appear to co‑localize, the results indicated that AMPK controls VEGF in EGCG‑treated cells regardless of the p53 status.

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