Abstract |
This study characterized the role of endoplasmic reticulum stress (ERS)-related pathways in arsenic trioxide-induced apoptosis in multidrug-resistant leukemia K562/ADM cells. Arsenic trioxide exposure led to much significant induction of apoptosis in K562/ADM cells than the parental K562 cells, and the chaperone proteins glucose-regulated protein 78, CHOP/GADD153, X-box binding protein-1 and caspase-12 were activated to varying degrees. Furthermore, arsenic trioxide stimulation led to inhibition of P-glycoprotein and Bcl-2 expression. This study demonstrates a missing link between arsenic trioxide and ERS-induced apoptosis, and suggests that the greater effects obtained in drug-resistant K562/ADM cells may be mediated by downregulation of P-glycoprotein and Bcl-2 expression.
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Authors | Jing Chen, Hulai Wei, Bei Xie, Bei Wang, Juan Cheng, Jie Cheng |
Journal | Leukemia research
(Leuk Res)
Vol. 36
Issue 12
Pg. 1526-35
(Dec 2012)
ISSN: 1873-5835 [Electronic] England |
PMID | 22959511
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2012 Elsevier Ltd. All rights reserved. |
Chemical References |
- ATP Binding Cassette Transporter, Subfamily B, Member 1
- Antineoplastic Agents
- Arsenicals
- DDIT3 protein, human
- DNA-Binding Proteins
- Endoplasmic Reticulum Chaperone BiP
- Growth Inhibitors
- Heat-Shock Proteins
- Oxides
- Proto-Oncogene Proteins c-bcl-2
- Regulatory Factor X Transcription Factors
- Transcription Factors
- Transcription Factor CHOP
- Caspase 12
- Arsenic Trioxide
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Topics |
- ATP Binding Cassette Transporter, Subfamily B, Member 1
(genetics, metabolism)
- Antineoplastic Agents
(pharmacology)
- Apoptosis
(drug effects)
- Arsenic Trioxide
- Arsenicals
(pharmacology)
- Caspase 12
(genetics, metabolism)
- DNA-Binding Proteins
(genetics, metabolism)
- Drug Resistance, Multiple
- Drug Resistance, Neoplasm
- Endoplasmic Reticulum
(drug effects, genetics, metabolism)
- Endoplasmic Reticulum Chaperone BiP
- Endoplasmic Reticulum Stress
(drug effects, genetics)
- Gene Expression Regulation, Neoplastic
- Growth Inhibitors
(pharmacology)
- Heat-Shock Proteins
(genetics, metabolism)
- Humans
- K562 Cells
- Oxides
(pharmacology)
- Proto-Oncogene Proteins c-bcl-2
(genetics, metabolism)
- Regulatory Factor X Transcription Factors
- Signal Transduction
- Transcription Factor CHOP
(genetics, metabolism)
- Transcription Factors
(genetics, metabolism)
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