The Effect of Survivin on Multidrug Resistance Mediated by P-Glycoprotein in MCF-7 and Its Adriamycin Resistant Cells
Although anticancer chemotherapeutic drugs have been designed to inhibit the growth of tumor cells, chemotherapy frequently fails due to the development of multidrug resistance (MDR). In this paper, the effect of survivin on multidrug resistance mediated by P-glycoprotein (Pgp) was investigated in b...
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| Published in | Biological & Pharmaceutical Bulletin Vol. 30; no. 12; pp. 2279 - 2283 |
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| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
Japan
The Pharmaceutical Society of Japan
01.12.2007
Pharmaceutical Society of Japan Japan Science and Technology Agency |
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| Online Access | Get full text |
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| Abstract | Although anticancer chemotherapeutic drugs have been designed to inhibit the growth of tumor cells, chemotherapy frequently fails due to the development of multidrug resistance (MDR). In this paper, the effect of survivin on multidrug resistance mediated by P-glycoprotein (Pgp) was investigated in breast cancer cells. Overexpression of survivin in MCF-7 cells transfected with survivin expression vector pEGFP/survivin results in decreasing sensitivity to anticancer drugs and activation of Pgp to export drug out of cells. Down regulation of survivin in MCF-7/adriamycin (ADR) transfected with RNAi directed against survivin vector psh1/survivin could increase the drug accumulation in cells by inhibiting Pgp. Downregulation of the expression of the Pgp with the specific inhibitor verapamil could markedly suppress the survivin mRNA expression, whereas the reverse impact was not observed. Survivin might modulate the turnover of Pgp or transport by Pgp in cells, which result in anti-apoptosis and drug resistance. Our results suggest that survivin might play a key role in MDR in the presence of Pgp, and this might represent a novel strategy for modulating MDR in cancer cells. |
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| AbstractList | Although anticancer chemotherapeutic drugs have been designed to inhibit the growth of tumor cells, chemotherapy frequently fails due to the development of multidrug resistance (MDR). In this paper, the effect of survivin on multidrug resistance mediated by P-glycoprotein (Pgp) was investigated in breast cancer cells. Over-expression of survivin in MCF-7 cells transfected with survivin expression vector pEGFP/survivin results in decreasing sensitivity to anticancer drugs and activation of Pgp to export drug out of cells. Down regulation of survivin in MCF-7/adriamycin (ADR) transfected with RNAi directed against survivin vector psh1/survivin could increase the drug accumulation in cells by inhibiting Pgp. Downregulation of the expression of the Pgp with the specific inhibitor verapamil could markedly suppress the survivin mRNA expression, whereas the reverse impact was not observed. Survivin might modulate the turnover of Pgp or transport by Pgp in cells, which result in antiapoptosis and drug resistance. Our results suggest that survivin might play a key role in MDR in the presence of Pgp, and this might represent a novel strategy for modulating MDR in cancer cells. Although anticancer chemotherapeutic drugs have been designed to inhibit the growth of tumor cells, chemotherapy frequently fails due to the development of multidrug resistance (MDR). In this paper, the effect of survivin on multidrug resistance mediated by P-glycoprotein (Pgp) was investigated in breast cancer cells. Overexpression of survivin in MCF-7 cells transfected with survivin expression vector pEGFP/survivin results in decreasing sensitivity to anticancer drugs and activation of Pgp to export drug out of cells. Down regulation of survivin in MCF-7/adriamycin (ADR) transfected with RNAi directed against survivin vector psh1/survivin could increase the drug accumulation in cells by inhibiting Pgp. Downregulation of the expression of the Pgp with the specific inhibitor verapamil could markedly suppress the survivin mRNA expression, whereas the reverse impact was not observed. Survivin might modulate the turnover of Pgp or transport by Pgp in cells, which result in anti-apoptosis and drug resistance. Our results suggest that survivin might play a key role in MDR in the presence of Pgp, and this might represent a novel strategy for modulating MDR in cancer cells. Although anticancer chemotherapeutic drugs have been designed to inhibit the growth of tumor cells, chemotherapy frequently fails due to the development of multidrug resistance (MDR). In this paper, the effect of survivin on multidrug resistance mediated by P-glycoprotein (Pgp) was investigated in breast cancer cells. Overexpression of survivin in MCF-7 cells transfected with survivin expression vector pEGFP/survivin results in decreasing sensitivity to anticancer drugs and activation of Pgp to export drug out of cells. Down regulation of survivin in MCF-7/adriamycin (ADR) transfected with RNAi directed against survivin vector psh1/survivin could increase the drug accumulation in cells by inhibiting Pgp. Downregulation of the expression of the Pgp with the specific inhibitor verapamil could markedly suppress the survivin mRNA expression, whereas the reverse impact was not observed. Survivin might modulate the turnover of Pgp or transport by Pgp in cells, which result in anti-apoptosis and drug resistance. Our results suggest that survivin might play a key role in MDR in the presence of Pgp, and this might represent a novel strategy for modulating MDR in cancer cells.Although anticancer chemotherapeutic drugs have been designed to inhibit the growth of tumor cells, chemotherapy frequently fails due to the development of multidrug resistance (MDR). In this paper, the effect of survivin on multidrug resistance mediated by P-glycoprotein (Pgp) was investigated in breast cancer cells. Overexpression of survivin in MCF-7 cells transfected with survivin expression vector pEGFP/survivin results in decreasing sensitivity to anticancer drugs and activation of Pgp to export drug out of cells. Down regulation of survivin in MCF-7/adriamycin (ADR) transfected with RNAi directed against survivin vector psh1/survivin could increase the drug accumulation in cells by inhibiting Pgp. Downregulation of the expression of the Pgp with the specific inhibitor verapamil could markedly suppress the survivin mRNA expression, whereas the reverse impact was not observed. Survivin might modulate the turnover of Pgp or transport by Pgp in cells, which result in anti-apoptosis and drug resistance. Our results suggest that survivin might play a key role in MDR in the presence of Pgp, and this might represent a novel strategy for modulating MDR in cancer cells. |
| Author | Liu, Feng Jiang, Yu-Yang Xie, Zhen-Hua Cai, Guo-Ping |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/18057712$$D View this record in MEDLINE/PubMed |
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| References_xml | – reference: 14) Tran J., Master Z., Yu J. L., Rak J., Dumont D. J., Kerbel R. S., Proc. Natl. Acad. Sci. U.S.A., 99, 4349—4354 (2002). – reference: 7) Tamm I., Wang Y., Sausville E., Scudiero D. A., Vigna N., Oltersdorf T., Reed J. C., Cancer Res., 58, 5315—5320 (1998). – reference: 28) Ling X., Yang J., Tan D. F., Ramnath N., Younis T., Bundy B. N., Slocum H. K., Yang L. L., Zhou M. X., Li F. Z., Lung Cancer, 49, 353—361 (2005). – reference: 10) O'Connor D. S., Grossman D., Plescia J., Li F., Zhang H., Villa A., Tognin S., Marchisio P. C., Altieri D. C., Proc. Natl. Acad. Sci. U.S.A., 97, 13103—13107 (2000). – reference: 17) Ikeguchi M., Liu J., Kaibara N., Apoptosis, 7, 23—29 (2002). – reference: 22) Monzo M., Rosell R., Felip E., Astudillo J., Sanchez J. J., Maestre J., Martin C., Font A., Barnadas A., Abad A., J. Clin. Oncol., 17, 2100—2104 (1999). – reference: 5) Li F., Ambrosini G., Chu E. Y., Plescia J., Tognin S., Marchisio P. C., Altieri D. C., Nature (London), 396, 580—584 (1998). – reference: 29) Dohi T., Beltrami E., Wall N. R., Plescia J., Altieri D. C., J. Clin. Invest., 114, 1117—1127 (2004). – reference: 4) Ambrosini G., Adida C., Altieri D. C., Nat. Med., 3, 917—921 (1997). – reference: 26) Cornwell M. M., Pastan I., Gottesman M. M., J. Biol. Chem., 262, 2166—2170 (1987). – reference: 27) Muller C., Goubin F., Ferrandis E., Mol. Pharmacol., 47, 51—56 (1995). – reference: 23) Tirro E., Consoli M. L., Massimino M., Manzella L., Frasca F., Sciacca L., Vicari L., Stassi G., Messina L., Messina A., Vigneri P., Cancer Res., 66, 4263—4272 (2006). – reference: 8) Deveraux Q. L., Reed J. C., Genes Dev., 13, 239—252 (1999). – reference: 11) Song Z., Yao X., Wu M., J. Biol. Chem., 278, 23130—23140 (2003). – reference: 12) Altieri D. C., J. Cell Biochem., 92, 656—663 (2004). – reference: 25) Nakagawa Y., Abe S., Kurata M., Hasegawa M., Yamamoto K., Inoue M., Takemura T., Suzuki K., Kitagawa M., Am. J. Hematol., 81, 824—831 (2006). – reference: 30) Rodriguez J. A., Span S. W., Ferreira C. G. M., Kruyt F. A. E., Giaccone G., Exp. Cell Res., 275, 44—53 (2002). – reference: 13) Zhang M., Latham D. E., Delaney M. A., Chakravarti A., Oncogene, 24, 2474—2482 (2005). – reference: 19) Ambudkar S. V., Kimchi-Sarfaty C., Sauna Z. E., Gottesman M. M., Oncogene, 22, 7468—7485 (2003). – reference: 9) Shin S., Sung B. J., Cho Y. S., Kim H. J., Ha N. C., Hwang J. I., Chung C. W., Jung Y. K., Oh B. H., Biochemistry, 40, 1117—1123 (2001). – reference: 15) Rodel C., Haas J., Groth A., Grabenbauer G. G., Sauer R., Rodel F., Int. J. Radiat. Oncol. Biol. Phys., 55, 1341—1347 (2003). – reference: 20) Nooter K., Herweijer H., Br. J. Cancer, 63, 663—669 (1991). – reference: 6) LaCasse E. C., Baird S., Korneluk R. G., MacKenzie A. 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| SubjectTerms | ATP Binding Cassette Transporter, Subfamily B, Member 1 - metabolism Cell Line, Tumor Cysteine Proteinase Inhibitors - pharmacology Doxorubicin - pharmacology Drug Resistance, Multiple Drug Resistance, Neoplasm Genetic Vectors Humans Inhibitor of Apoptosis Proteins MCF-7 cell Microtubule-Associated Proteins - biosynthesis Microtubule-Associated Proteins - genetics Microtubule-Associated Proteins - pharmacology multidrug resistance Neoplasm Proteins - biosynthesis Neoplasm Proteins - genetics Neoplasm Proteins - pharmacology P-glycoprotein Plasmids - genetics RNA, Messenger - biosynthesis RNA, Messenger - genetics Survivin Transfection |
| Title | The Effect of Survivin on Multidrug Resistance Mediated by P-Glycoprotein in MCF-7 and Its Adriamycin Resistant Cells |
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