Please use this identifier to cite or link to this item: https://doi.org/10.1002/mc.20487
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dc.titlePolyporenic acid C induces caspase-8-mediated apoptosis in human lung cancer A549 cells
dc.contributor.authorLing, H.
dc.contributor.authorZhou, L.
dc.contributor.authorJia, X.
dc.contributor.authorGapter, L.A.
dc.contributor.authorAgarwal, R.
dc.contributor.authorNg, K.-Y.
dc.date.accessioned2014-05-19T02:54:10Z
dc.date.available2014-05-19T02:54:10Z
dc.date.issued2009-06
dc.identifier.citationLing, H., Zhou, L., Jia, X., Gapter, L.A., Agarwal, R., Ng, K.-Y. (2009-06). Polyporenic acid C induces caspase-8-mediated apoptosis in human lung cancer A549 cells. Molecular Carcinogenesis 48 (6) : 498-507. ScholarBank@NUS Repository. https://doi.org/10.1002/mc.20487
dc.identifier.issn08991987
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/53096
dc.description.abstractLung cancer continues to be the leading cause of cancer-related mortality worldwide. This warrants the search for new and effective agents against lung cancer. We and others have recently shown that lanostane-type triterpenoids isolated from the fungal species Poria cocos (P. cocos) can inhibit cancer growth. However, the mechanisms responsible for the anticancer effects of these triterpenoids remain unclear. In this study, we investigated the effect of polyporenic acid C (PPAC), a lanostane-type triterpenoid from P. cocos, on the growth of A549 nonsmall cell lung cancer cells (NSCLC). The results demonstrate that PPAC significantly reduced cell proliferation via induction of apoptosis as evidenced by sub-G1 analysis, annexin V-FITC staining, and increase in cleavage of procaspase-8, -3, and poly(ADP-ribose)-polymerase (PARP). However, unlike our previously reported lanostane-type triterpenoid, pachymic acid, treatment of cells with PPAC was not accompanied by disruption of mitochondrial membrane potential and increase in cleavage of procaspase-9. Further, PPC-induced apoptosis was inhibited by caspase-8 and pan caspase inhibitors but not by a caspase-9 inhibitor. Taken together, the results suggest that PPAC induces apoptosis through the death receptor-mediated apoptotic pathway where the activation of caspase-8 leads to the direct cleavage of execution caspases without the involvement of the mitochondria. Furthermore, suppressed PI3-kinase/Akt signal pathway and enhanced p53 activation after PPAC treatment suggests this to be an additional mechanism for apoptosis induction. Together, these results encourage further studies of PPAC as a promising candidate for lung cancer therapy. © 2008 Wiley-Liss, Inc.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1002/mc.20487
dc.sourceScopus
dc.subjectAkt
dc.subjectApoptosis
dc.subjectCaspase-8
dc.subjectJNK
dc.subjectLung cancer
dc.subjectp53
dc.subjectPARP
dc.subjectPolyporenic acid C
dc.subjectPoria cocos
dc.typeArticle
dc.contributor.departmentPHARMACY
dc.contributor.departmentBIOLOGICAL SCIENCES
dc.description.doi10.1002/mc.20487
dc.description.sourcetitleMolecular Carcinogenesis
dc.description.volume48
dc.description.issue6
dc.description.page498-507
dc.description.codenMOCAE
dc.identifier.isiut000266473600003
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