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Enhancement of paclitaxel-induced breast cancer cell death via the glycogen synthase kinase-3 beta-mediated B-cell lymphoma 2 regulation

Author(s)
Noh, Kyung TaeCha, Gil SunKang, Tae HeungCho, JoonJung, In DukKim, Kwang-YounAhn, Soon-CheolYou, Ji ChangPark, Yeong-Min
Issued Date
2016-01
DOI
10.5483/BMBRep.2016.49.1.102
URI
https://scholarworks.unist.ac.kr/handle/201301/19075
Fulltext
http://koreascience.or.kr/article/ArticleFullRecord.jsp?cn=E1MBB7_2016_v49n1_51
Citation
BMB REPORTS, v.49, no.1, pp.51 - 56
Abstract
Glycogen synthase kinase-3 beta (GSK-3 beta) is a serine/threonine protein kinase that is known to mediate cancer cell death. Here, we show that B-cell lymphoma 2 (Bcl-2), an anti-apoptotic protein, is regulated by GSK-3 beta and that GSK-3 beta-mediated regulation of Bcl-2 is crucial for mitochondrial-dependent cell death in paclitaxel-stimulated cells. We demonstrate that MCF7 GSK3 beta siRNA cells are more sensitive to cell death than MCF7 GFP control cells and that in the absence of GSK-3 beta, Bcl-2 levels are reduced, a result enhanced by paclitaxel. Paclitaxel-induced JNK (c-Jun N-terminal kinase) activation is critical for Bcl-2 modulation. In the absence of GSK-3 beta, Bcl-2 was unstable in an ubiquitination-dependent manner in both basal-and paclitaxel-treated cells. Furthermore, we demonstrate that GSK-3 beta-mediated regulation of Bcl-2 influences cytochrome C release and mitochondrial membrane potential. Taken together, our data suggest that GSK-3 beta-dependent regulation of Bcl-2 is crucial for mitochondria-dependent cell death in paclitaxel-mediated breast cancer therapy.
Publisher
KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
ISSN
1976-6696
Keyword (Author)
B-cell lymphoma 2Breast cancerCell deathGlycogen synthase kinase-3 betaPaclitaxel
Keyword
PROTEIN-KINASEAPOPTOSISTAXOLPROMOTESSURVIVALPATHWAYMICROTUBULESREQUIREMENTACTIVATIONINHIBITION

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