TGF-[beta]1-induced epithelial-mesenchymal transition and acetylation of Smad2 and Smad3 are negatively regulated by EGCG in Human A549 lung cancer cells

Highlights * EGCG inhibited acetylation of Smad2 and Smad3 by p300/CBP during TGF-b1-induced EMT, and EGCG is a strong HAT inhibitor. * EGCG suppressed the TGF-b1-induced EMT related genes. * EGCG antagonizes the migration of human lung cancer cells permitted by TGF-b1-induced EMT. * EGCG is directl...

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Veröffentlicht in:	Cancer letters 2013-07, Vol.335 (1), p.205
Hauptverfasser:	Ko, Hyeonseok, So, Youngsin, Jeon, Hyelin, Jeong, Mi-Hyeon, Choi, Hyo-Kyoung, Ryu, Seung-Hee, Lee, Sang-Wook, Yoon, Ho-Geun, Choi, Kyung-Chul
Format:	Artikel
Sprache:	eng
Schlagworte:	Antibiotics Apoptosis Cell adhesion & migration Chromatin Disease prevention Epigenetics Gene expression Kinases Morphology Phosphorylation Polyphenols Proteins Rodents Studies
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Beschreibung
Zusammenfassung:	Highlights * EGCG inhibited acetylation of Smad2 and Smad3 by p300/CBP during TGF-b1-induced EMT, and EGCG is a strong HAT inhibitor. * EGCG suppressed the TGF-b1-induced EMT related genes. * EGCG antagonizes the migration of human lung cancer cells permitted by TGF-b1-induced EMT. * EGCG is directly prevented EMT and blocked invasion and metastasis of cancer cells.
ISSN:	0304-3835 1872-7980
DOI:	10.1016/j.canlet.2013.02.018