期刊
ONCOLOGY LETTERS
卷 6, 期 5, 页码 1346-1350出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/ol.2013.1533
关键词
p53; vascular endothelial growth factor; matrix metalloproteinase-9; migration-suppressing effects; epigallocatechin-3-gallate
类别
资金
- National Research Foundation of Korea [KRF-2012-0021402]
- Korea Science and Engineering Foundation (KOSEF)
- Korean government (MEST) [R01-2008-000-20131-0]
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-a. 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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