[fe3o4磁性纳米颗粒对卵巢癌细胞多药耐药的逆转作用及其与凋亡相关基因的相关性]。

Zhi Jiang, Bao-An Chen, Qiang Wu, Guo-Hua Xia, Yu Zhang, Feng Gao, Tie-Yan Hong, Cui-Rong Xu, Jian Cheng, Guo-Hong Li, Wen-Ji Chen, Li-Jie Liu, Xiao-Mao Li, Xue-Mei Wang
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引用次数: 8

摘要

背景与目的:顺铂耐药(DDP)是卵巢癌成功治疗的主要障碍。本研究旨在研究fe3o4磁性纳米颗粒(MNPs)对卵巢癌细胞株SKOV3/DDP耐药的逆转作用,并探讨其与凋亡相关基因的相关性。方法:将SKOV3/DDP细胞分为DDP组、Fe3O4-MNPs组、DDP + Fe3O4-MNPs组和对照组。MTT法检测细胞增殖情况。流式细胞术检测细胞凋亡情况。采用电感耦合等离子体原子发射光谱法(ICP-AES)检测细胞内DDP水平。逆转录聚合酶链反应(RT-PCR)检测凋亡相关基因、bcl-2和survivin的表达。结果:Fe3O4-MNPs使SKOV3/DDP细胞的DDP抗性逆转2.259倍。联合用药组细胞凋亡率和细胞内DDP水平均显著高于DDP组(结论:Fe3O4-MNPs可逆转卵巢癌SKOV3/DDP细胞的DDP耐药,其作用可能与下调bcl-2和survivin的表达有关。
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[Reversal effect of Fe3O4-magnetic nanoparticles on multi-drug resistance of ovarian carcinoma cells and its correlation with apoptosis-associated genes].

Background and objective: Resistance to cisplatin (DDP) remains a major obstacle for the successful treatment of ovarian cancer. This study was to determine the reversal effect of Fe3O4-magnetic nanoparticles (MNPs) on DDP-resistance of ovarian carcinoma cell line SKOV3/DDP, and to explore its correlation with apoptosis-associated genes.

Methods: SKOV3/DDP cells were divided into the DDP group, the Fe3O4-MNPs group, the combination (DDP plus Fe3O4-MNPs) group, and the control group. Cell proliferation was determined by MTT assay. Cell apoptosis was analyzed by flow cytometry (FCM). Intracellular DDP level was detected by inductively coupled plasma atomic emission spectrometry (ICP-AES). The expressions of apoptosis-associated genes, bcl-2, and survivin were detected by reverse transcription-polymerase chain reaction (RT-PCR).

Results: Fe3O4-MNPs reversed DDP-resistance of SKOV3/DDP cells by 2.259 folds. The cell apotosis rate and the intracellular DDP level were significantly higher in the combination group than in the DDP group (P<0.05). Moreover, the mRNA levels of bcl-2 and survivin were significantly lower in the combination group than in the DDP group(P<0.05).

Conclusions: Fe3O4-MNPs can reverse the DDP resistance of ovarian carcinoma SKOV3/DDP cells, and the effect may be ascribed to the down-regulation of bcl-2 and survivin expression.

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