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Suppression of NRF2/ARE by convallatoxin sensitises A549 cells to 5-FU-mediated apoptosis
- Authors
- Lee, June; Kang, Jong-Su; Nam, Le Ba; Yoo, Ok-Kyung; Keum, Young-Sam
- Issue Date
- 2-Dec-2018
- Publisher
- TAYLOR & FRANCIS LTD
- Keywords
- 5-Fluorouracil (5-FU); antioxidant response element (ARE); convallatoxin; NRF2
- Citation
- FREE RADICAL RESEARCH, v.52, no.11-12, pp 1416 - 1423
- Pages
- 8
- Indexed
- SCI
SCIE
SCOPUS
- Journal Title
- FREE RADICAL RESEARCH
- Volume
- 52
- Number
- 11-12
- Start Page
- 1416
- End Page
- 1423
- ISSN
- 1071-5762
1029-2470
- Abstract
- NF-E2-related factor 2 (NRF2) regulates transcription of phase II cytoprotective enzymes to protect normal cells against oxidative stress. However, a high level of NRF2 offers a growth advantage, chemoresistance, and radioresistance in cancer. In the present study, we have identified convallatoxin as a novel inhibitor of NRF2/ARE. Suppression of NRF2 by convallatoxin was not transcriptionally mediated, but regulated at the level of proteolysis. Convallatoxin activated GSK-3 beta and suppression of NRF2 by convallatoxin required the Neh6 domain. Convallatoxin sensitised A549 cells to 5-fluorouracil-mediated cell death by promoting apoptosis. Together, our results provide evidence that convallatoxin might be useful as a chemotherapeutic adjuvant due to its ability to suppress NRF2/ARE.
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Related Researcher
- Keum, Young Sam
- College of Pharmacy (Department of Pharmacy)