The establishment of two paclitaxel‐resistant prostate cancer cell lines and the mechanisms of paclitaxel resistance with two cell lines

Takeda, Masatoshi; Mizokami, Atsushi; Mamiya, Kiminori; Li, You Qiang; Zhang, Jian; Keller, Evan T.; Namiki, Mikio

doi:10.1002/pros.20581

Cited by 135 publications

(190 citation statements)

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“…Due to recent reports of decreased methylation of the downstream ABCB1 promoter in association with drug resistance, [4][5][6][7]10,25 we next investigated this mechanism as the possible cause of increased ABCB1 expression in our drug-resistant cell lines. Most of the variation in the degree of promoter methylation within drug-sensitive cell lines (including MCF-7 DOX-2 , MCF-7 EPI and MCF-7 TAX-2 cells selected to dose-8 and MCF-7 CC cells 'selected' to dose-12) occurred within the first 30 CpG sites (Figures 3d and 5a), which is consistent with the bisulfite sequencing data for MCF-7 cells reported by David et al 8 Significantly decreased methylation of the ABCB1 downstream promoter was observed in MCF-7 EPI cells at the onset of drug resistance (selection dose-9) both in terms of average promoter methylation (Figure 3a) and methylation across specific CpG sites (Figures 3e and 5c).…”

Section: Discussionmentioning

confidence: 99%

“…In particular, the ABCB1 promoter has been shown to be hypomethylated in several drug-resistant sub-lines of human leukemia (CCRF-CEM and HL60), 4,5 human epidermoid (KB3-1) 6 and prostate cancer (DU145) cells. 7 Similarly, one study examined differences in methylation between the ABCB1 5 0 -untranslated regions of drug-resistant and drugsensitive breast cancer cells. 8 This study established a correlation between increased ABCB1 expression and hypomethylation of the ABCB1 promoter by comparing the methylation of CpG dinucleotides within the ABCB1 downstream promoters of MCF-7 and MCF-7/ADR cells.…”

Section: Introductionmentioning

confidence: 99%

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The temporal relationship between ABCB1 promoter hypomethylation, ABCB1 expression and acquisition of drug resistance

et al. 2010

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Induced expression of the Abcb1 drug transporter often occurs in tumors in response to chemotherapy. The role that epigenetic modifications within the ABCB1 promoter play in Abcb1 expression remains unclear. We selected MCF-7 cells for survival in increasing doses of chemotherapy drugs, and assessed the methylation status of 66 CpG sites within the ABCB1 promoter preceding, accompanying and following the onset of drug resistance. Increased ABCB1 transcript expression coincident with acquisition of resistance to epirubicin or paclitaxel was temporally associated with hypomethylation of the ABCB1 downstream promoter in the absence of gene amplifications or changes in mRNA stability. Treatment of control MCF-7 cells with demethylating and/or acetylating agents increased ABCB1 transcript expression. In addition to broad promoter hypomethylation, dramatic reductions in the methylation of specific CpG sites within the promoter were observed, suggesting that these sites may play a predominant role in transcriptional activation through promoter hypomethylation. Furthermore, our data suggest that allele-specific reductions in ABCB1 promoter methylation regulate promoter usage within paclitaxel-resistant cells. This study provides strong evidence that changes in ABCB1 promoter methylation, ABCB1 promoter usage and ABCB1 transcript expression can be temporally and causally correlated with the acquisition of drug resistance in breast tumor cells.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The temporal relationship between ABCB1 promoter hypomethylation, ABCB1 expression and acquisition of drug resistance

et al. 2010

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“…Several taxane resistant cell lines have been generated in lung, ovarian, prostatic, breast, and gastric cancers (Chu et al 2000 ;Okugawa et al 2004;Duan et al 2005;Takeda et al 2007;Zhang et al 2010). However, establishment of esophageal cancer is limited; only a single study has been reported (Wang et al 2013).…”

Section: Discussionmentioning

confidence: 99%

ABCB1 Is Upregulated in Acquisition of Taxane Resistance: Lessons from Esophageal Squamous Cell Carcinoma Cell Lines

Wang

Sumarpo

Saiki

et al. 2016

Tohoku J. Exp. Med.

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Esophageal cancer is one of the common malignancies worldwide, particularly in eastern African and Asian countries including Japan. Taxane (paclitaxel or docetaxel) is one of the effective chemotherapeutic reagents for patients with esophageal cancer, but acquisition of chemoresistance frequently occurs; this is one of the most frequent causes for therapeutic failure. In this study, we established three taxane resistant esophageal squamous cell carcinoma cell lines and explored possible mechanisms for the acquisition of chemoresistance. Microarray analyses indicated that the ABCB1 (ATP binding cassette subfamily B member 1) gene was significantly upregulated in taxane resistant esophageal cancer cell lines. Moreover, we found that siRNA mediated ABCB1 knockdown successfully restored drug sensitivity in both paclitaxel and docetaxel resistant esophageal cancer cell lines. In conclusion, we propose that ABCB1 might play a pivotal role in acquisition of taxane resistance and could be a promising target for treatment of patients with esophageal cancer after acquisition of taxane resistance.

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“…4B) The PC-3 cells were chosen to test whether these differences in efflux could be caused by different ABC transporters being responsible for the efflux of marizomib and NPI-0047. This cell line was used for this study because it is known to express members of the MRP family of multidrug efflux pumps (Zalcberg et al, 2000;Takeda et al, 2007). As a positive control to confirm the presence of an MRP efflux transporter, the cells were incubated for 1 h with 5 M fluorescein, a known MRP substrate, in the absence or presence of …”

Section: Evaluation Of Proteasome Inhibition Bymentioning

confidence: 99%

Proteasome Regulator Marizomib (NPI-0052) Exhibits Prolonged Inhibition, Attenuated Efflux, and Greater Cytotoxicity than Its Reversible Analogs

Obaidat

Weiss²,

Wahlgren³

et al. 2011

J Pharmacol Exp Ther

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The present study was undertaken to compare the cellular transport characteristics of [ 3 H]NPI-0052 (1R,4R,5S)-4-(2-.0]heptane-3,7-dione in RPMI 8226 multiple myeloma and PC-3 prostate adenocarcinoma cells to determine whether these properties explain differences in the cytotoxic potencies of these chemical analogs. The results indicate that marizomib, which possesses a chemicalleaving group, is more cytotoxic to both cell lines and inhibits proteasome activity more completely at lower concentrations than NPI-0047, a nonleaving-group analog. Moreover, it was found that both compounds accumulate in these cells by simple diffusion and the same carrier-mediated transport system. Although the rate of uptake is similar, the cellular efflux, which does not seem to be mediated by a major ATP-binding cassette (ABC)-efflux transporter, is more rapid for NPI-0047 than for marizomib. Experiments revealed that the irreversible binding of marizomib to the proteasome is responsible for its slower efflux, longer duration of action, and greater cytotoxicity compared with NPI-0047. The discovery that major ABC transporters of the multidrug resistance-associated protein family do not seem to be involved in the accumulation or removal of these agents suggests they may not be affected by multidrug resistance mechanisms during prolonged administration.

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The establishment of two paclitaxel‐resistant prostate cancer cell lines and the mechanisms of paclitaxel resistance with two cell lines

Abstract: Background. Although paclitaxel is used for hormone-resistant prostate cancer, relapse

Cited by 135 publications

References 33 publications

The temporal relationship between ABCB1 promoter hypomethylation, ABCB1 expression and acquisition of drug resistance

The temporal relationship between ABCB1 promoter hypomethylation, ABCB1 expression and acquisition of drug resistance

ABCB1 Is Upregulated in Acquisition of Taxane Resistance: Lessons from Esophageal Squamous Cell Carcinoma Cell Lines

Proteasome Regulator Marizomib (NPI-0052) Exhibits Prolonged Inhibition, Attenuated Efflux, and Greater Cytotoxicity than Its Reversible Analogs

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