L-type calcium channel blockers reverse docetaxel and vincristine-induced multidrug resistance independent of ABCB1 expression in human lung cancer cell lines.

doi:10.1016/j.toxlet.2009.11.018

中山醫學大學機構典藏 CSMUIR > 醫學院 > 免疫學研究所 > 期刊論文 > Item 310902500/11741

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题名:	L-type calcium channel blockers reverse docetaxel and vincristine-induced multidrug resistance independent of ABCB1 expression in human lung cancer cell lines.
作者:	Chiu, LY Ko, JL Lee, YJ Yang, TY Tee, YT Sheu, GT
贡献者:	中山醫學大學
关键词:	Multidrug resistance;ATP-binding cassette transporter;Docetaxel;Vincristine;Calcium channel blocker;Verapamil
日期:	2010
上传时间:	2015-07-28T09:32:02Z (UTC)
ISSN:	0378-4274
摘要:	Multidrug resistance (MDR) of cancer cells to cytotoxic drugs significantly impedes chemotherapeutic treatment. The purpose of this study is to characterize docetaxel (DOC) or vincristine (VCR) selected A549 and H1299 non-small cell lung cancer (NSCLC) sublines that exhibit MDR phenotypes and followed by re-sensitization study. Although all drug resistant sublines showed cross-resistance to DOC, VCR, and doxorubicin (DXR), the expression of ATP-binding cassette (ABC) transporter B1 (ABCB1) gene was found to be strongly induced in DOC but not in VCR resistant A549 sublines by quantitative reverse transcription real-time polymerase chain reaction (qRT-PCR). In DOC and VCR resistant H1299 sublines, moderate expression of ABCB1 was detected. The levels of ABCB1 protein and efflux activities were further examined by immunoblotting and rhodamin-123 staining assay. The results showed that both ABC and non-ABC mediated MDR are existed. Furthermore, verapamil (VER), an inhibitor of ABCB1 and an L-type calcium channel blocker, is capable of reversing the resistance in all drug-resistant sublines independent of ABCB1 expression. Importantly, VER only sensitizes resistant sublines but has no effect on parental cancer cells. Other L-type calcium channel blockers, such as diltiazem (DIL) and nifedipine (NIF), also sensitize MDR sublines without interfering with ABCB1 activity but with lower efficacy than VER. Our data showed that in addition to ABCB1, calcium channel activity may play a crucial role in DOC- and VCR-acquired MDR. Therefore, inhibition of calcium influx may provide a new target to modulate MDR in chemotherapy. Copyright 2009 Elsevier Ireland Ltd. All rights reserved.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/11741 http://dx.doi.org/10.1016/j.toxlet.2009.11.018
關聯:	Toxicol Lett. 2010 Feb 15;192(3):408-18.
显示于类别:	[免疫學研究所] 期刊論文

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