Induction of hypoxia-inducible factor-1a inhibits drug-induced apoptosis in the human leukemic cell line HL-60open access
- Authors
- Yook, Yeon-Joo; Seo, Young-Jin; Kang, Hyoung Jin; Ko, Sang-Hyeok; Shin, Hee Young; Lee, Jeong Jin; Jeong, Gajin; Ahn, Hyo Seop
- Issue Date
- Sep-2010
- Publisher
- 대한혈액학회
- Keywords
- Hypoxia; Arsenic trioxide; HIF-1a; Cobalt chloride; Bax; HSP70
- Citation
- Blood Research, v.45, no.3, pp 158 - 163
- Pages
- 6
- Journal Title
- Blood Research
- Volume
- 45
- Number
- 3
- Start Page
- 158
- End Page
- 163
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/57768
- DOI
- 10.5045/kjh.2010.45.3.158
- ISSN
- 2287-979X
2288-0011
- Abstract
- Background Leukemic cells originate from hypoxic bone marrow, which protects them from anti-cancer drugs. Although many factors that cause drug resistance in leukemic cells have been studied, the effect of hypoxia on drug-induced apoptosis is still poorly understood.
Methods In this study, we examined the effect of hypoxia on anti-leukemic drug resistance in leukemic cell lines treated with cobalt chloride (CoCl2), a hypoxia-mimetic agent. Cellular proliferation was evaluated using the methyl thiazolyl tetrazolium (MTT) assay. Flow cytometry analysis and western blots were performed to investigate apoptosis-related proteins. Results Unlike its previously known apoptotic effect, the expression of HIF-1a increased the survival rate of human promyelocytic leukemia HL-60 cells when these cells were exposed to anti-leukemic drugs; these effects were mediated by heat-shock protein HSP70 and the pro-apoptotic protein Bax. Conclusion These findings may provide new insights for understanding the mechanisms underlying hypoxia and for designing new therapeutic strategies for acute myeloid leukemia.
- Files in This Item
-
- Appears in
Collections - College of Natural Sciences > Department of Life Science > 1. Journal Articles
![qrcode](https://api.qrserver.com/v1/create-qr-code/?size=55x55&data=https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/57768)
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.