The establishment of two paclitaxel-resistant prostate cancer cell lines and the mechanisms of paclitaxel resistance with two cell lines
dc.contributor.author | Takeda, Masashi | en_US |
dc.contributor.author | Mizokami, Atsushi | en_US |
dc.contributor.author | Mamiya, Kiminori | en_US |
dc.contributor.author | Li, You Qiang | en_US |
dc.contributor.author | Zhang, Jian | en_US |
dc.contributor.author | Keller, Evan T. | en_US |
dc.contributor.author | Namiki, Mikio | en_US |
dc.date.accessioned | 2007-09-20T18:27:14Z | |
dc.date.available | 2008-09-08T14:25:13Z | en_US |
dc.date.issued | 2007-06-15 | en_US |
dc.identifier.citation | Takeda, Masashi; Mizokami, Atsushi; Mamiya, Kiminori; Li, You Qiang; Zhang, Jian; Keller, Evan T.; Namiki, Mikio (2007)."The establishment of two paclitaxel-resistant prostate cancer cell lines and the mechanisms of paclitaxel resistance with two cell lines." The Prostate 67(9): 955-967. <http://hdl.handle.net/2027.42/56002> | en_US |
dc.identifier.issn | 0270-4137 | en_US |
dc.identifier.issn | 1097-0045 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/56002 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=17440963&dopt=citation | en_US |
dc.description.abstract | BACKGROUND Although paclitaxel is used for hormone-resistant prostate cancer, relapse definitely occurs later. Details of the molecular mechanism responsible for paclitaxel- resistance remain unclear. METHODS We established paclitaxel-resistant cells, DU145-TxR and PC-3-TxR from parent DU145 and PC-3. To characterize these cells, we examined cross-resistance to other anticancer drugs. Expression of several potential genes that had been related to drug-resistance was compared with parent cells by RT-PCR and Western blotting. Methylation analysis of multiple drug resistance (MDR1) promoter was carried out using bisulfite-modified DNA from cell lines. Knockdown experiments using small interfering RNA (siRNA) were also performed to confirm responsibility of drug-resistance. Finally, cDNA microarray was performed to quantify gene expression in PC-3 and PC-3-TxR cells. RESULTS The IC 50 for paclitaxel in DU145-TxR and PC-3-TxR was 34.0- and 43.4-fold higher than that in both parent cells, respectively. Both cells showed cross-resistance to some drugs, but not to VP-16 and cisplatin. Methylation analysis revealed that methylated CpG sites of MDR1 promoter in DU145 and PC-3 cells were demethylated in DU145-TxR cells, but not in PC-3-TxR cells. Knockdown of P-glycoprotein (P-gp), which was up-regulated in resistant cells, by MDR-1 siRNA restored paclitaxel sensitivity in DU145-TxR but not in PC-3-TxR, indicating that up-regulation of P-gp was not always main cause of paclitaxel-resistance. Microarray analysis identified 201 (1.34%) up-regulated genes and 218 (1.45%) out of screened genes in PC-3-TxR. CONCLUSIONS Our data will provide molecular mechanisms of paclitaxel-resistance and be useful for screening target genes to diagnose paclitaxel sensitivity. Prostate 67: 955–967, 2007. © 2007 Wiley-Liss, Inc. | en_US |
dc.format.extent | 472545 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | Wiley Subscription Services, Inc., A Wiley Company | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Cancer Research, Oncology and Pathology | en_US |
dc.title | The establishment of two paclitaxel-resistant prostate cancer cell lines and the mechanisms of paclitaxel resistance with two cell lines | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Internal Medicine and Specialties | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Unit for Laboratory Animal Medicine and Department of Pathology, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationother | Department of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, Japan | en_US |
dc.contributor.affiliationother | Department of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, Japan ; Department of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Sciences, 13-1 Takara-machi, Kanazawa, Ishikawa 920-8640, Japan. | en_US |
dc.contributor.affiliationother | Department of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, Japan | en_US |
dc.contributor.affiliationother | Department of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, Japan | en_US |
dc.contributor.affiliationother | Department of Medicine, Division of Hematology/Oncology, University Drive, Pittsburgh | en_US |
dc.contributor.affiliationother | Department of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, Japan | en_US |
dc.identifier.pmid | 17440963 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/56002/1/20581_ftp.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1002/pros.20581 | en_US |
dc.identifier.source | The Prostate | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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