Publication:
Epibrassinolide alters PI3K/MAPK signaling axis via activating Foxo3a-induced mitochondria-mediated apoptosis in colon cancer cells

dc.contributor.authorÇoker Gürkan, Ajda
dc.contributor.authorPalavan Unsal, Narcin
dc.contributor.authorARISAN, ELİF DAMLA
dc.contributor.authorYERLİKAYA, PINAR OBAKAN
dc.contributor.authorCOŞKUN, DENİZ
dc.contributor.authorID156421tr_TR
dc.contributor.authorID113920tr_TR
dc.contributor.authorID125860tr_TR
dc.date.accessioned2018-07-12T07:19:54Z
dc.date.available2018-07-12T07:19:54Z
dc.date.issued2015-10-15
dc.description.abstractEpibrassinolide (EBR), a steroid-derived plant growth regulator, has been recently suggested as an apoptotic inducer in different cancer cells. In this experimental study, we investigated the potential apoptotic effect of EBR on stress-related and survival signaling molecules in colon carcinoma cells. EBR decreased cell viability and colony formation in HCT 116 and HT-29 colon carcinoma cells. The inactivation of PI3K/AKT by EBR treatment led to upregulation of Foxo3a, which in turn induced apoptosis in HCT 116 and HT-29 cells. In addition, the upstream non-receptor protein tyrosine kinase Src was found elevated allowing to the upregulation of p38, stress-activated protein kinase/Jun amino-terminal kinase and extracellular signal-regulated kinase 1/2 and their target genes c-jun, c-fos and c-myc in a time-dependent manner in HCT 116 cells within 48 h. The alterations in PA metabolism caused intracellular PA pool decrease. The upregulation of pro-apoptotic Bak, Bax, Puma and Bim were accompanied with the decrease in Mcl-1 in HCT 116 and Bcl-x(L), expression profiles in HT-29 following 48 h EBR treatment. We suggest that the upregulation of Bim expression levels might be related with one of the PI3K/AKT target transcription factor Foxo3a, which was dephosphorylated by EBR treatment in HCT 116 and HT-29 cells. (C) 2015 Elsevier Inc. All rights reserved.tr_TR
dc.identifier.issn0014-4827
dc.identifier.other1090-2422
dc.identifier.pubmed26318418
dc.identifier.pubmed26318418en
dc.identifier.scopus2-s2.0-84942199756
dc.identifier.scopus2-s2.0-84942199756en
dc.identifier.urihttps://doi.org/10.1016/j.yexcr.2015.08.015
dc.identifier.urihttps://hdl.handle.net/11413/2023
dc.identifier.wos362999100002
dc.identifier.wos362999100002en
dc.language.isoen_UStr_TR
dc.publisherElsevier Inc, 525 B Street, Ste 1900, San Diego, Ca 92101-4495 Usatr_TR
dc.relationExperimental Cell Researchtr_TR
dc.subjectEpibrassinolidetr_TR
dc.subjectPolyaminestr_TR
dc.subjectApoptosistr_TR
dc.subjectColon cancertr_TR
dc.subjectPI3Ktr_TR
dc.subjectAKTtr_TR
dc.subjectFoxo3atr_TR
dc.subjectForkhead Transcription Factortr_TR
dc.subjectPolyamine Catabolismtr_TR
dc.subjectCycle Arresttr_TR
dc.subjectMap Kinasestr_TR
dc.subjectPathwaystr_TR
dc.subjectJnktr_TR
dc.subjectP53tr_TR
dc.subjectBrassinosteroidstr_TR
dc.subjectInhibitiontr_TR
dc.subjectExpressiontr_TR
dc.titleEpibrassinolide alters PI3K/MAPK signaling axis via activating Foxo3a-induced mitochondria-mediated apoptosis in colon cancer cellstr_TR
dc.typeArticle
dspace.entity.typePublication
local.indexed.atpubmed
local.indexed.atscopus
local.indexed.atwos
relation.isAuthorOfPublication3d33e154-a50c-46b8-ad6e-25a26bf11cf0
relation.isAuthorOfPublication387670e2-5a88-4937-b3da-1dda9aedfbdd
relation.isAuthorOfPublication44df5e00-bc42-470a-98e0-12025ec91466
relation.isAuthorOfPublication.latestForDiscovery3d33e154-a50c-46b8-ad6e-25a26bf11cf0

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