Tumor suppressive roles of eugenol in human lung cancer cells

Background Eugenol, a natural compound available in Syzigium aromaticum (cloves), is exploited for various medicinal applications. Eugenol induces apoptosis and functions as an anti‐cancer drug in several types of tumors. We investigated the tumor suppressive role and potential mechanisms of eugenol...

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Bibliographic Details
Published inThoracic cancer Vol. 9; no. 1; pp. 25 - 29
Main Authors Fangjun, Li, Zhijia, Yang
Format Journal Article
LanguageEnglish
Published Melbourne John Wiley & Sons Australia, Ltd 01.01.2018
John Wiley & Sons, Inc
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Summary:Background Eugenol, a natural compound available in Syzigium aromaticum (cloves), is exploited for various medicinal applications. Eugenol induces apoptosis and functions as an anti‐cancer drug in several types of tumors. We investigated the tumor suppressive role and potential mechanisms of eugenol in human lung cancer cells. Methods Human embryonic lung fibroblast MRC‐5 and lung cancer adenocarcinoma A549 cells were incubated with or without various concentrations of eugenol for 24 hours. Cell counting kit 8 and crystal violet staining assays were performed to detect cell viability. The cell migration and invasion abilities were also determined by wound healing and transwell assays. Finally, Western blotting assay was performed to examine the changes in lung cancer cell viability and invasion of downstream targets after treatment with eugenol. Results Eugenol could inhibit cell viability in lung cancer cells. Furthermore, eugenol obviously impaired cell migration and invasion. Finally, the expression levels of phosphate‐Akt and MMP‐2 in lung cancer cells were reduced after treatment with eugenol. Conclusion Our results demonstrated the tumor suppressive roles of eugenol on lung cancer cell proliferation, migration, and invasion partially through the PI3K/Akt pathway and MMP activity in vitro. These results suggest eugenol as a potential chemotherapeutic agent against human lung cancer.
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Both authors contributed equally to this work.
ISSN:1759-7706
1759-7714
1759-7714
DOI:10.1111/1759-7714.12508