[KSCI] Korea Science Citation Index Service

http://dx.doi.org/10.5483/BMBRep.2016.49.1.102

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

Noh, Kyung Tae (Department of Infectious Diseases, Armed Forces Medical Research Institute)
Cha, Gil Sun (Department of Immunology, KU Open Innovation Center, College of Medicine, Konkuk University)
Kang, Tae Heung (Department of Immunology, KU Open Innovation Center, College of Medicine, Konkuk University)
Cho, Joon (Department of Neurosurgery, Konkuk University Hospital)
Jung, In Duk (Department of Immunology, KU Open Innovation Center, College of Medicine, Konkuk University)
Kim, Kwang-Youn (School of Life Sciences, Ulsan National Institute of Science and Technology)
Ahn, Soon-Cheol (Department of Microbiology and Immunology, Pusan National University School of Medicine)
You, Ji Chang (National Research Laboratory of Molecular Virology, epartment of Pathology, School of Medicine, The Catholic University of Korea)
Park, Yeong-Min (Department of Immunology, KU Open Innovation Center, College of Medicine, Konkuk University)

Publication Information

BMB Reports / v.49, no.1, 2016 , pp. 51-56 More about this Journal

Abstract

Glycogen synthase kinase-3β (GSK-3β) 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-3β and that GSK-3β-mediated regulation of Bcl-2 is crucial for mitochondrial-dependent cell death in paclitaxel-stimulated cells. We demonstrate that MCF7 GSK-3β siRNA cells are more sensitive to cell death than MCF7 GFP control cells and that in the absence of GSK-3β, 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-3β, Bcl-2 was unstable in an ubiquitination-dependent manner in both basal- and paclitaxel-treated cells. Furthermore, we demonstrate that GSK-3β-mediated regulation of Bcl-2 influences cytochrome C release and mitochondrial membrane potential. Taken together, our data suggest that GSK-3β-dependent regulation of Bcl-2 is crucial for mitochondria-dependent cell death in paclitaxel-mediated breast cancer therapy. [BMB Reports 2016; 49(1): 51-56]

Keywords

B-cell lymphoma 2; Breast cancer; Cell death; Glycogen synthase kinase-3β; Paclitaxel;

Citations & Related Records

Times Cited By KSCI : 3 (Citation Analysis)

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