5-Caffeoylquinic acid inhibits invasion of non-small cell lung cancer cells through the inactivation of p70S6K and Akt activity: Involvement of p53 in differential regulation of signaling pathways

被引:30
作者
In, Jae-Kyung [1 ]
Kim, Jin-Kyu [2 ]
Oh, Joa Sub [1 ]
Seo, Dong-Wan [1 ]
机构
[1] Dankook Univ, Dept Pharm, Coll Pharm, Cheonan 31116, South Korea
[2] Gyeonggi Inst Sci & Technol Promot, Bioctr, Suwon 16229, South Korea
关键词
5-caffeoylquinic acid; invasion; non-small cell lung cancer; p53; p70(S6K); Akt; GROWTH-FACTOR RECEPTOR; MATRIX METALLOPROTEINASES; SIEGESBECKIA-GLABRESCENS; TISSUE INHIBITORS; DOWN-REGULATION; PROLIFERATION; MIGRATION; ANGIOGENESIS; SUPPRESSION; EXPRESSION;
D O I
10.3892/ijo.2016.3436
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
In the present study, we investigated the effects and molecular mechanism of 5-caffeoylquinic acid (5-CQA), a natural phenolic compound isolated from Ligularia fischeri, on cell invasion, proliferation and adhesion in p53 wild-type A549 and p53-deficient H1299 non-small cell lung cancer (NSCLC) cells. 5-CQA abrogated mitogen-stimulated invasion, but not proliferation, in both A549 and H1299 cells. In addition, 5-CQA inhibited mitogen-stimulated adhesion in A549 cells only. Anti-invasive activity of 5-CQA in A549 cells was mediated by the inactivation of p70(S6K)-dependent signaling pathway. In contrast, in H1299 cells the inactivation of Akt was found to be involved in 5-CQA-mediated inhibition of cell invasion. Collectively, these findings demonstrate the pharmacological roles and molecular targets of 5-CQA in regulating NSCLC cell fate, and suggest further evaluation and development of 5-CQA as a potential therapeutic agent for the treatment and prevention of lung cancer.
引用
收藏
页码:1907 / 1912
页数:6
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