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MOLECULAR BIOLOGICAL EVIDENCES FOR THE GENETIC STABILITY OF DOXORUBICIN RESISTANT CELL LINE S-180R IN VIVO

MOLECULAR BIOLOGICAL EVIDENCES FOR THE GENETIC STABILITY OF DOXORUBICIN RESISTANT CELL LINE S 180R IN VIVO
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摘要 Objective: In order to assess the genetic stability of doxorubicin resistance sarcoma S 180R cell line in vivo . Methods: The drug resistant genes and molecules were examined by flow cytometry, Southern blot, Northern blot and RT PCR. Results: The results showed that drug efflux in S 180R increased nearly 100 folds, as compared with its parent cells, the rate of half peak width resistant cell/peak high decreased from 0.56 to 0.23 measured by flow cytometry after two years. The mdr1 gene amplified and overexpressed significantly in S 180R and the expression of topoisomerase II α gene decreased remarkably in S 180R. There was no significant different of the MRP expression between S 180R and S 180. Conclusion: These results indicated that drug resistance of S 180R was maintained and also increased. The major mechanism of drug resistance is the amplification and overexpression of mdr1 gene, the decreased expression of topoisomerase II α also contributed to it. So, S 180R is an ideal experimental model for the study of doxorubicin resistance and its reversion in vivo . Objective: In order to assess the genetic stability of doxorubicin resistance sarcoma S 180R cell line in vivo . Methods: The drug resistant genes and molecules were examined by flow cytometry, Southern blot, Northern blot and RT PCR. Results: The results showed that drug efflux in S 180R increased nearly 100 folds, as compared with its parent cells, the rate of half peak width resistant cell/peak high decreased from 0.56 to 0.23 measured by flow cytometry after two years. The mdr1 gene amplified and overexpressed significantly in S 180R and the expression of topoisomerase II α gene decreased remarkably in S 180R. There was no significant different of the MRP expression between S 180R and S 180. Conclusion: These results indicated that drug resistance of S 180R was maintained and also increased. The major mechanism of drug resistance is the amplification and overexpression of mdr1 gene, the decreased expression of topoisomerase II α also contributed to it. So, S 180R is an ideal experimental model for the study of doxorubicin resistance and its reversion in vivo .
出处 《Chinese Journal of Cancer Research》 SCIE CAS CSCD 1998年第3期33-36,共4页 中国癌症研究(英文版)
关键词 Multidrug resistance DOXORUBICIN S 180R Topo II . Multidrug resistance, Doxorubicin, S 180R, Topo II .
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