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| Content Provider | PubMed Central |
|---|---|
| Author | Teraishi, Fuminori Zhang, Lidong Guo, Wei Dong, Fengqin Davis, John J. Lin, Anning Fang, Bingliang |
| Abstract | Although gemcitabine is a potent therapeutic agent in the treatment of human non-small cell lung cancer (NSCLC), resistance to gemcitabine is common. In this study, we investigated the molecular mechanisms involved in acquired gemcitabine resistance against NSCLC cells. Gemcitabine-resistant NSCLC H1299 cells (H1299/GR) were selected by long-term exposure of parental H1299 cells to gemcitabine. The median inhibitory concentrations of gemcitabine in H1299 and H1299/GR cells were 19.4 nM and 233.1 nM, respectively. Gemcitabine induced activation of JNK in parental H1299 cells but not in H1299/GR cells after 48 h. Blocking JNK activation by pretreatment with SP600125, a specific JNK inhibitor, or by transfection with dominant-negative JNK vectors abrogated gemcitabine-induced apoptosis in parental H1299 cells as evidenced by interruption of caspase activation. Transient transfection with a JNKK2-JNK1 plasmid expressing constitutive JNK1 partially restored the effect of gemcitabine in H1299/GR cells. Our results indicate that gemcitabine-induced apoptosis in human NSCLC H1299 cells requires activation of the JNK signaling pathway. Attenuated JNK activation may contribute to development of acquired gemcitabine resistance in cancer cells. |
| Related Links | http://dx.doi.org/10.1016/j.febslet.2005.10.064 |
| Ending Page | 6687 |
| Page Count | 7 |
| Starting Page | 6681 |
| File Format | |
| ISSN | 00145793 |
| Journal | FEBS letters |
| Issue Number | 29 |
| Volume Number | 579 |
| Language | English |
| Publisher Date | 2005-12-05 |
| Access Restriction | Open |
| Subject Keyword | Biophysics Genetics Cell Biology Biochemistry Molecular Biology Structural Biology Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Genetics Structural Biology Biochemistry Molecular Biology Biophysics |
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