Abstract | BACKGROUND & OBJECTIVE: METHODS: RESULTS: HIF-1alpha expression was inhibited at both mRNA and protein levels after transfection of RNAi HIF-1alpha, which subsequently caused a dramatic decrease in VEGF, Glut-1, PGK, and P-gp under hypoxic conditions. In addition, HIF-1alpha inhibition was found to increase drug sensitivity of K562 cells to HHT. CONCLUSION: HIF-1alpha inhibition may result in a decrease of genes related to angiogenesis and glycolysis metabolism and an increase of drug sensitivity to HHT in K562 cells.
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Authors | Bing-Zong Li, Wen-Zhuo Zhuang, Ping Chen, Jin-Xiang Fu |
Journal | Ai zheng = Aizheng = Chinese journal of cancer
(Ai Zheng)
Vol. 27
Issue 7
Pg. 723-8
(Jul 2008)
China |
PMID | 18606065
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antineoplastic Agents, Phytogenic
- Glucose Transporter Type 1
- HIF1A protein, human
- Harringtonines
- Hypoxia-Inducible Factor 1, alpha Subunit
- Vascular Endothelial Growth Factor A
- Homoharringtonine
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Topics |
- Antineoplastic Agents, Phytogenic
(pharmacology)
- Base Sequence
- Glucose Transporter Type 1
(biosynthesis)
- Harringtonines
(pharmacology)
- Homoharringtonine
- Humans
- Hypoxia-Inducible Factor 1, alpha Subunit
(antagonists & inhibitors, genetics)
- K562 Cells
- Leukemia, Myelogenous, Chronic, BCR-ABL Positive
(drug therapy, metabolism)
- Molecular Sequence Data
- RNA Interference
- Vascular Endothelial Growth Factor A
(metabolism)
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