| Title |
|
|
|
Multidrug-resistance in rat colon-carcinoma cell-lines CC531, and cc531(rev)
| |
| Author |
|
|
|
| |
| Abstract |
|
|
|
| A rat colon carcinoma cell line, CC531, was exposed to stepwise increasing concentrations of colchicine. A cell line, CC531mdr+, which grows in the presence of 0.2 muM of colchicine was obtained. A revertant cell line, CC531rev was isolated upon colchicine withdrawal. The CC531mdr+ displayed a multidrug-resistant phenotype. Marked resistance to the selecting agent colchicine, was found (RF=37.5) as well as to vinblastine (RF=11.3) and actinomycin D (RF=2.6). Cross resistance to doxorubicin (RF=8) and daunorubicin (RF=13.3) was demonstrated. Verapamil was able to reverse drug resistance to colchicine and daunorubicin. The revertant cell line, CC531rev, showed increased sensitivity to colchicine (RF=0.43), vinblastine (RF=0.13), doxorubicin (RF=0.28) and daunorubicin (RF=0.56). Marked cross resistance to cis-platinum (RF=6.9) was also induced in CC531mdr+ and was maintained in CC531rev. We conclude that CC531 displays an intrinsic low-level multidrug-resistant phenotype, which was amplified in the CC531mdr+ variant. This correlates with a higher level of expression of P-glycoprotein. CC531rev lacks the multidrug-resistant phenotype and can be used as the drug-sensitive counterpart of the latter two cell lines. Furthermore, it has been shown that in these cell lines cis-platinum resistance is mediated through a mechanism independent of the multidrug-resistant phenotype, since the revertant cell line CC531rev has lost the multidrug-resistant phenotype while retaining the concomitantly induced cis-platinum resistance of the multidrug-resistant variant CC531mdr+. | | |
| Language |
|
|
|
English
| |
| Source (journal) |
|
|
|
Japanese journal of cancer research / Japanese Cancer Association. - Tokyo | |
| Publication |
|
|
|
Tokyo : 1993
| |
| ISSN |
|
|
|
0910-5050
| |
| Volume/pages |
|
|
|
84:11(1993), p. 1201-1208
| |
| ISI |
|
|
|
A1993MH95600017
| |
| Full text (Publisher's DOI) |
|
|
| | |
| Full text (publisher's version - intranet only) |
|
|
| | |
|