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艾拉司群在卵巢癌的二维和三维细胞培养模型中抑制乳腺癌耐药蛋白(BCRP)的蛋白活性,并使细胞对细胞毒性药物重新敏感。

Elacridar Inhibits BCRP Protein Activity in 2D and 3D Cell Culture Models of Ovarian Cancer and Re-Sensitizes Cells to Cytotoxic Drugs.

作者信息

Stasiak Piotr, Sopel Justyna, Płóciennik Artur, Musielak Oliwia, Lipowicz Julia Maria, Rawłuszko-Wieczorek Agnieszka Anna, Sterzyńska Karolina, Korbecki Jan, Januchowski Radosław

机构信息

Institute of Biological Sciences, Faculty of Exact and Natural Sciences, University of Zielona Góra, 65-417 Zielona Góra, Poland.

The Doctoral School of Exact and Technical Sciences, University of Zielona Góra, 65-417 Zielona Góra, Poland.

出版信息

Int J Mol Sci. 2025 Jun 17;26(12):5800. doi: 10.3390/ijms26125800.

Abstract

Chemotherapy resistance is a major obstacle in the treatment of ovarian cancer, often resulting in disease recurrence and poor prognosis for patients. A key contributor to this resistance is the overexpression of ATP-binding cassette (ABC) transporters, including breast cancer resistance protein (BCRP/ABCG2), which actively effluxes chemotherapeutic agents such as topotecan (TOP) or mitoxantrone (MIT), limiting their intracellular accumulation and efficacy. This study investigated the potential of elacridar (GG918), a potent dual P-gp and BCRP inhibitor, to overcome drug resistance in ovarian cancer cell lines. Both TOP-sensitive and TOP-resistant ovarian cancer cells were grown in two-dimensional (2D) monolayers and three-dimensional (3D) spheroid models to better mimic the tumor microenvironment. The expression of the ABCG2 gene was quantified via qPCR and BCRP protein levels were assessed by western blotting and immunofluorescence. Drug response was evaluated using MTT viability assays, while BCRP transporter activity was examined using flow cytometry and microscopic assessment of the intracellular retention of BCRP fluorescent substrates (Hoechst 33342 and MIT). In both 2D and 3D cultures, elacridar effectively inhibited BCRP function and significantly enhanced sensitivity to TOP. These findings suggest that elacridar can inhibit BCRP-mediated drug resistance in ovarian cancer cell models.

摘要

化疗耐药是卵巢癌治疗中的主要障碍,常导致疾病复发和患者预后不良。这种耐药的一个关键因素是ATP结合盒(ABC)转运蛋白的过表达,包括乳腺癌耐药蛋白(BCRP/ABCG2),它能主动外排拓扑替康(TOP)或米托蒽醌(MIT)等化疗药物,限制它们在细胞内的蓄积及其疗效。本研究调查了强效的P-糖蛋白和BCRP双重抑制剂艾拉司群(GG918)克服卵巢癌细胞系耐药的潜力。TOP敏感和TOP耐药的卵巢癌细胞在二维(2D)单层培养和三维(3D)球体模型中生长,以更好地模拟肿瘤微环境。通过qPCR定量ABCG2基因的表达,并用蛋白质印迹法和免疫荧光法评估BCRP蛋白水平。使用MTT活力测定评估药物反应,同时使用流式细胞术和对BCRP荧光底物(Hoechst 33342和MIT)细胞内潴留的显微镜评估来检测BCRP转运蛋白活性。在2D和3D培养中,艾拉司群均有效抑制BCRP功能并显著增强对TOP的敏感性。这些发现表明,艾拉司群可在卵巢癌细胞模型中抑制BCRP介导的耐药。

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