Please use this identifier to cite or link to this item: https://doi.org/10.1002/mc.20597
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dc.titlePachymic acid inhibits cell growth and modulates arachidonic acid metabolism in nonsmall cell lung cancer A549 cells
dc.contributor.authorLing, H.
dc.contributor.authorJia, X.
dc.contributor.authorZhang, Y.
dc.contributor.authorGapter, L.A.
dc.contributor.authorLim, Y.-S.
dc.contributor.authorAgarwal, R.
dc.contributor.authorNg, K.-Y.
dc.date.accessioned2014-10-27T08:36:09Z
dc.date.available2014-10-27T08:36:09Z
dc.date.issued2010-03
dc.identifier.citationLing, H., Jia, X., Zhang, Y., Gapter, L.A., Lim, Y.-S., Agarwal, R., Ng, K.-Y. (2010-03). Pachymic acid inhibits cell growth and modulates arachidonic acid metabolism in nonsmall cell lung cancer A549 cells. Molecular Carcinogenesis 49 (3) : 271-282. ScholarBank@NUS Repository. https://doi.org/10.1002/mc.20597
dc.identifier.issn08991987
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/101343
dc.description.abstractAberrant arachidonic acid (AA) metabolism has been involved in inflammation and carcinogenesis. The key enzymes in AA metabolism such as cytosolic phospholipase A2 (cPLA2) and cyclooxygenase-2 (COX-2) have been implicated in the development and progression of many human cancers, including lung cancer. Hence, the blockade of these enzymes may suppress promotion and survival of human cancer cells. We and others have shown that a natural triterpenoid, pachymic acid (PA), can exhibit antiinflammatory and anticancer properties; however, its potential mechanism has not been fully clarified. In this study, we examined the effect of PA on the proliferation of human nonsmall cell lung cancer A549 cells. Furthermore, we investigated the influences of nontoxic levels of PA on AA metabolism. Additionally, the cellular events and signal transduction pathways influenced by PA were also examined. Our results showed that PA (1) inhibited anchorage-dependent and -independent A549 growth in a concentration-dependent manner, (2) induced apoptosis and disrupted mitochondrial membrane potential in A549 cells, and at nonlethal levels, (3) decreased IL-1β-induced activation of cPLA2 and COX-2, (4) suppressed IL-1β-induced activation of mitogen-activated protein kinases (MAPKs), and (5) inhibited IL-1β-stimulated nuclear factor kappa B (NF-κB) signaling pathways. We speculate that inhibition of AA metabolism by PA is mediated in part by its inhibition of MAPKs and NF-κB signaling pathways. Our study reveals that, apart from its cytotoxic effect, PA has the chemopreventive potential by reducing production of eicosanoids from AA metabolism. © 2009 Wiley-Liss, Inc.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1002/mc.20597
dc.sourceScopus
dc.subjectCOX-2
dc.subjectcPLA2
dc.subjectMAPK
dc.subjectNF-κB
dc.subjectPachymic acid
dc.typeArticle
dc.contributor.departmentPHARMACY
dc.contributor.departmentBIOLOGICAL SCIENCES
dc.description.doi10.1002/mc.20597
dc.description.sourcetitleMolecular Carcinogenesis
dc.description.volume49
dc.description.issue3
dc.description.page271-282
dc.description.codenMOCAE
dc.identifier.isiut000275216500007
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