Please use this identifier to cite or link to this item: https://ir.swu.ac.th/jspui/handle/123456789/13306
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dc.contributor.authorSophonnithiprasert T.
dc.contributor.authorMahabusarakam W.
dc.contributor.authorNakamura Y.
dc.contributor.authorWatanapokasin R.
dc.date.accessioned2021-04-05T03:23:11Z-
dc.date.available2021-04-05T03:23:11Z-
dc.date.issued2017
dc.identifier.issn17921074
dc.identifier.other2-s2.0-85003874459
dc.identifier.urihttps://ir.swu.ac.th/jspui/handle/123456789/13306-
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85003874459&doi=10.3892%2fol.2016.5381&partnerID=40&md5=354b690e042d6eb1ab40b3e990a93797
dc.description.abstractGoniothalamin, a natural occurring styryl-lactone isolated from Goniothalamus macrophyllus (Blume) Hook. f. & Thomson var. macrophyllus, can trigger cancer cell death in various types of cancer cell. The present study focused on elucidation of the mitochondria-mediated apoptosis associated with endoplasmic reticulum (ER) stress-induced activation of c-Jun NH2-terminal kinase (JNK) by goniothalamin in HeLa cervical cancer cells. Cell viability was determined using an MTT assay, and DNA condensation and loss of mitochondrial membrane potential were determined using Hoechst 33342 and JC-1 staining, respectively. Flow cytometry was used for cell cycle and phosphatidyl-serine exposure analyses. Apoptotic-associated ER stress signaling pathways were determined using immunoblotting, reverse transcription-polymerase chain reaction (RT-PCR) and RT-quantitative PCR analyses. The results suggested that goniothalamin suppressed cell proliferation in a time-and dose-dependent manner. The induction of apoptosis was confirmed by increased DNA condensation, loss of mitochondrial membrane potential and cell surface phosphatidyl-serine presentation. The cell cycle analysis demonstrated that the goniothalamin-treated HeLa cells were in G2/M arrest. Determination of the caspase cascade and apoptotic proteins indicated the induction of apoptosis through the intrinsic pathway. In addition, the levels of phosphorylated JNK and the transcription factor, C/EBP homologous protein (CHOP), an ER stress-associated apoptotic molecule, were increased in the goniothalamin-treated cells. These data indicated that goniothalamin exerted a cytotoxic effect against HeLa cells via the induction of mitochondria-mediated apoptosis, associated with ER stress-induced activation of JNK. © 2017, Spandidos Publications. All rights reserved.
dc.subjectglucose regulated protein 78
dc.subjectmitogen activated protein kinase 1
dc.subjectmitogen activated protein kinase 3
dc.subjectprotein bcl 2
dc.subjectprotein p53
dc.subjectstress activated protein kinase
dc.subjectapoptosis
dc.subjectArticle
dc.subjectcell cycle parameters
dc.subjectcell proliferation
dc.subjectcontrolled study
dc.subjectcytotoxicity
dc.subjectdisorders of mitochondrial functions
dc.subjectendoplasmic reticulum stress
dc.subjectflow cytometry
dc.subjectHeLa cell line
dc.subjecthuman
dc.subjecthuman cell
dc.subjectIC50
dc.subjectmitochondrial membrane potential
dc.subjectMTT assay
dc.subjectpolyacrylamide gel electrophoresis
dc.subjectreverse transcription polymerase chain reaction
dc.subjectsignal transduction
dc.subjectspectrophotometry
dc.titleGoniothalamin induces mitochondria-mediated apoptosis associated with endoplasmic reticulum stress-induced activation of JNK in HeLa cells
dc.typeArticle
dc.rights.holderScopus
dc.identifier.bibliograpycitationOncology Letters. Vol 13, No.1 (2017), p.119-128
dc.identifier.doi10.3892/ol.2016.5381
Appears in Collections:Scopus 1983-2021

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