Abstract
Using the patch-clamp method, we investigated a relationship between MDR1 expression and its effects on the CFTR channel function. Incubation of CaCo-2 cells with increasing concentrations of doxorubicin resulted in a reduction of CFTR chloride channel activity in a dose-dependent manner. This reduction was associated with a decrease of CFTR mRNA and simultaneous up-regulation of MDR1 mRNA in the presence of doxorubicin. Similar alteration of the CFTR function was observed in CaCo-2 cells transiently overexpressing MDR1. No alterations of the cAMP-dependent chloride currents were observed in COS-1 cells transiently co-expressing CFTR and MDR1 from strong CMV promoters. This indicated that repression of CFTR by MDR1 induction requires the presence of the native CFTR promoter. © 2003 Elsevier Science (USA). All rights reserved.
| Original language | English |
|---|---|
| Pages (from-to) | 248-252 |
| Number of pages | 4 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 304 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 2 May 2003 |
Keywords
- cAMP-activated chloride channel
- CFTR
- Co-expression
- Cystic fibrosis
- Doxorubicin
- MDR1
- Multidrug resistance
- Patch-clamp technique