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Inhibition of glutamine utilization sensitizes lung cancer cells to apigenin-induced apoptosis resulting from metabolic and oxidative stress

Authors
 Yoon-Mi Lee  ;  Gibok Lee  ;  Taek-In Oh  ;  Byeong Mo Kim  ;  Do-Wan Shim  ;  Kwang-Ho Lee  ;  Young Jun Kim  ;  Beong Ou Lim  ;  Ji-Hong Lim 
Citation
 INTERNATIONAL JOURNAL OF ONCOLOGY, Vol.48(1) : 399-408, 2016 
Journal Title
 INTERNATIONAL JOURNAL OF ONCOLOGY 
ISSN
 1019-6439 
Issue Date
2016
Abstract
Recent studies have shown anticancer activity of apigenin by suppressing glucose transporter 1 (GLUT1) expression in cultured cancer cells; however, it is not clear whether apigenin can suppress glucose metabolism in lung cancer cells or sensitize them to inhibition of glutamine utilization-mediated apoptosis through metabolic and oxidative stress. We show that apigenin significantly decreases GLUT1 expression in mice. Furthermore, we demonstrate that apigenin induces growth retardation and apoptosis through metabolic and oxidative stress caused by suppression of glucose utilization in lung cancer cells. The underlying mechanisms were defined that the anticancer effects of apigenin were reversed by ectopic GLUT1 overexpression and galactose supplementation, through activation of pentose phosphate pathway-mediated NADPH generation. Importantly, we showed that severe metabolic stress using a glutaminase inhibitor, compound 968, was involved in the mechanism of sensitization by apigenin. Taken together, the combination of apigenin with inhibitors of glutamine metabolism may provide a promising therapeutic strategy for cancer treatment.
Files in This Item:
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DOI
10.3892/ijo.2015.3243
Appears in Collections:
5. Research Institutes (연구소) > Yonsei Integrative Research Institute for Cerebral & Cardiovascular Disease (뇌심혈관질환융합연구사업단) > 1. Journal Papers
Yonsei Authors
Kim, Byeong Mo(김병모) ORCID logo https://orcid.org/0000-0002-0582-3132
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/155726
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