Abstract |
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.
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Authors | Jae-Kyung In, Jin-Kyu Kim, Joa Sub Oh, Dong-Wan Seo |
Journal | International journal of oncology
(Int J Oncol)
Vol. 48
Issue 5
Pg. 1907-12
(May 2016)
ISSN: 1791-2423 [Electronic] Greece |
PMID | 26984670
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- TP53 protein, human
- Tumor Suppressor Protein p53
- caffeoylquinic acid
- Quinic Acid
- Proto-Oncogene Proteins c-akt
- Ribosomal Protein S6 Kinases, 70-kDa
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Topics |
- Carcinoma, Non-Small-Cell Lung
(drug therapy, metabolism)
- Cell Line, Tumor
- Cell Movement
(drug effects)
- Cell Proliferation
(drug effects)
- Gene Expression Regulation, Neoplastic
(drug effects)
- Humans
- Lung Neoplasms
(drug therapy, metabolism)
- Neoplasm Invasiveness
- Proto-Oncogene Proteins c-akt
(metabolism)
- Quinic Acid
(analogs & derivatives, pharmacology)
- Ribosomal Protein S6 Kinases, 70-kDa
(metabolism)
- Signal Transduction
(drug effects)
- Tumor Suppressor Protein p53
(metabolism)
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