Wu Chung-Pu, Lusvarghi Sabrina, Tseng Pin-Jung, Hsiao Sung-Han, Huang Yang-Hui, Hung Tai-Ho, Ambudkar Suresh V
Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University Tao-Yuan, Taiwan.
Department of Physiology and Pharmacology, College of Medicine, Chang Gung University Tao-Yuan, Taiwan.
Am J Cancer Res. 2020 Jan 1;10(1):164-178. eCollection 2020.
The overexpression of one or multiple ATP-binding cassette (ABC) transporters such as ABCB1, ABCC1 or ABCG2 in cancer cells often leads to the development of multidrug resistance phenotype and consequent treatment failure. Therefore, these transporters constitute an important target to improve the therapeutic outcome in cancer patients. In this study, we employed a drug repurposing approach to identify MY-5445, a known phosphodiesterase type 5 inhibitor, as a selective modulator of ABCG2. We discovered that by inhibiting the drug transport function of ABCG2, MY-5445 potentiates drug-induced apoptosis in ABCG2-overexpressing multidrug-resistant cancer cells and resensitizes these cells to chemotherapeutic drugs. Our data of MY-5445 stimulating the ATPase activity of ABCG2 and molecular docking analysis of its binding to the substrate-binding pocket of ABCG2 provide additional insight into the manner in which MY-5445 interacts with ABCG2. Furthermore, we found that ABCG2 does not confer resistance to MY-5445 in human cancer cells. Overall, our study revealed an additional action of MY-5445 to resensitize ABCG2-overexpressing multidrug-resistant cancer cells to conventional anticancer drugs, and this should be evaluated in future drug combination trials.
癌细胞中一种或多种ATP结合盒(ABC)转运蛋白(如ABCB1、ABCC1或ABCG2)的过表达通常会导致多药耐药表型的出现以及随之而来的治疗失败。因此,这些转运蛋白构成了改善癌症患者治疗效果的重要靶点。在本研究中,我们采用药物再利用方法,确定了一种已知的5型磷酸二酯酶抑制剂MY-5445作为ABCG2的选择性调节剂。我们发现,通过抑制ABCG2的药物转运功能,MY-5445增强了药物诱导的ABCG2过表达的多药耐药癌细胞的凋亡,并使这些细胞对化疗药物重新敏感。我们关于MY-5445刺激ABCG2的ATP酶活性的数据及其与ABCG2底物结合口袋结合的分子对接分析,为MY-5445与ABCG2相互作用的方式提供了更多见解。此外,我们发现ABCG2在人类癌细胞中不会赋予对MY-5445的耐药性。总体而言,我们的研究揭示了MY-5445的另一种作用,即使ABCG2过表达的多药耐药癌细胞对传统抗癌药物重新敏感,这一点应在未来的药物联合试验中进行评估。