Mechanism of miR-126 Loaded in Albumin Nanoparticles for Reversing the Multidrug Resistance in Breast Carcinoma Cells

IF 2.9 4区 医学 Q1 Medicine Journal of biomedical nanotechnology Pub Date : 2024-06-01 DOI:10.1166/jbn.2024.3845
Yang Zhang, Yiming Yang, Ning Li, Fen Hu, Faming Tian, Hao Dai, Haifeng Cai, Jinyin Yan
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Abstract

This study discussed the mechanism of miR-126 loaded in albumin nanoparticles in reversing the multi drug resistance (MDR) in breast carcinoma cells through EGFR-MEK-ERK signal pathway. MCF-7/ADM cells were divided into blank set, empty vector set, miR-126 set and set of vector and miR-126 randomly. The change of drug susceptibility, protein expression of P-gp, BCRP, EGFR, p-EGFR, MEK, p-MEK, ERK and p-ERK, correlation between miR-126 and EGFR-MEK- ERK signal pathway were observed. miR-126 expression in set of vector was the highest. The second was in miR-126 set. IC50 of ADM in miR-126 set was 4.6 µg/mL. The reversion times were two times. The reversion times in set of vector and miR-126 set was 2.8 times. The presentation of BCRP and P-gp in miR-126 set and set of vector and miR-126 was reduced notably. The activity of EGFR-MEK-ERK signal pathway was restrained by miR-126. The content of p-EGFR, p-MEK and p-ERK in miR-126 set and set of vector and miR-126 was reduced notably compared with blank set. EGFR-MEK-ERK signal activity was targeting regulated by miR-126 loaded in albumin nanoparticles. The level of phosphoric acid activators was reduced abnormally. The expression of BCRP and P-gp was reduced notably. The MDR in breast carcinoma cells was reversed and the drug susceptibility was elevated notably.
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载入白蛋白纳米颗粒的 miR-126 逆转乳腺癌细胞多药耐药性的机制
本研究探讨了载入白蛋白纳米颗粒的miR-126通过表皮生长因子受体-MEK-ERK信号通路逆转乳腺癌细胞多重耐药性(MDR)的机制。将 MCF-7/ADM 细胞随机分为空白组、空载体组、miR-126 组和载体与 miR-126 组。观察药物敏感性的变化、P-gp、BCRP、EGFR、p-EGFR、MEK、p-MEK、ERK 和 p-ERK 蛋白表达、miR-126 与 EGFR-MEK- ERK 信号通路的相关性。其次是 miR-126 组。miR-126 组中 ADM 的 IC50 为 4.6 µg/mL。逆转时间为两次。载体组和 miR-126 组的逆转时间为 2.8 倍。在 miR-126 组和载体与 miR-126 组中,BCRP 和 P-gp 的呈现明显减少。miR-126 抑制了表皮生长因子受体-MEK-ERK 信号通路的活性。与空白对照组相比,p-EGFR、p-MEK 和 p-ERK 在 miR-126 组和载体与 miR-126 组中的含量明显降低。载入白蛋白纳米颗粒的 miR-126 对表皮生长因子受体-MEK-ERK 信号活性具有靶向调节作用。磷酸激活剂的水平异常降低。BCRP 和 P-gp 的表达明显减少。乳腺癌细胞的 MDR 被逆转,对药物的敏感性显著提高。
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来源期刊
CiteScore
4.30
自引率
17.20%
发文量
145
审稿时长
2.3 months
期刊介绍: Information not localized
期刊最新文献
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