Frame I J, Deniskin Roman, Rinderspacher Alison, Katz Francine, Deng Shi-Xian, Moir Robyn D, Adjalley Sophie H, Coburn-Flynn Olivia, Fidock David A, Willis Ian M, Landry Donald W, Akabas Myles H
ACS Chem Biol. 2015 Mar 20;10(3):775-83. doi: 10.1021/cb500981y. Epub 2015 Jan 30.
Equilibrative transporters are potential drug targets; however, most functional assays involve radioactive substrate uptake that is unsuitable for high-throughput screens (HTS). We developed a robust yeast-based growth assay that is potentially applicable to many equilibrative transporters. As proof of principle, we applied our approach to Equilibrative Nucleoside Transporter 1 of the malarial parasite Plasmodium falciparum (PfENT1). PfENT1 inhibitors might serve as novel antimalarial drugs since PfENT1-mediated purine import is essential for parasite proliferation. To identify PfENT1 inhibitors, we screened 64 560 compounds and identified 171 by their ability to rescue the growth of PfENT1-expressing fui1Δ yeast in the presence of a cytotoxic PfENT1 substrate, 5-fluorouridine (5-FUrd). In secondary assays, nine of the highest activity compounds inhibited PfENT1-dependent growth of a purine auxotrophic yeast strain with adenosine as the sole purine source (IC50 0.2-2 μM). These nine compounds completely blocked [(3)H]adenosine uptake into PfENT1-expressing yeast and erythrocyte-free trophozoite-stage parasites (IC50 5-50 nM), and inhibited chloroquine-sensitive and -resistant parasite proliferation (IC50 5-50 μM). Wild-type (WT) parasite IC50 values were up to 4-fold lower compared to PfENT1-knockout (pfent1Δ) parasites. pfent1Δ parasite killing showed a delayed-death phenotype not observed with WT. We infer that, in parasites, the compounds inhibit both PfENT1 and a secondary target with similar efficacy. The secondary target identity is unknown, but its existence may reduce the likelihood of parasites developing resistance to PfENT1 inhibitors. Our data support the hypothesis that blocking purine transport through PfENT1 may be a novel and compelling approach for antimalarial drug development.
平衡型转运体是潜在的药物靶点;然而,大多数功能测定涉及放射性底物摄取,这不适用于高通量筛选(HTS)。我们开发了一种强大的基于酵母的生长测定法,该方法可能适用于许多平衡型转运体。作为原理验证,我们将我们的方法应用于疟原虫恶性疟原虫(PfENT1)的平衡型核苷转运体1。PfENT1抑制剂可能作为新型抗疟药物,因为PfENT1介导的嘌呤摄取对于寄生虫增殖至关重要。为了鉴定PfENT1抑制剂,我们筛选了64560种化合物,并通过它们在细胞毒性PfENT1底物5-氟尿苷(5-FUrd)存在下拯救表达PfENT1的fui1Δ酵母生长的能力鉴定出171种。在二次测定中,九种活性最高的化合物抑制了以腺苷为唯一嘌呤源的嘌呤营养缺陷型酵母菌株的PfENT1依赖性生长(IC50为0.2 - 2 μM)。这九种化合物完全阻断了[³H]腺苷摄取到表达PfENT1的酵母和无红细胞滋养体阶段寄生虫中(IC50为5 - 50 nM),并抑制了氯喹敏感和耐药寄生虫的增殖(IC50为5 - 50 μM)。野生型(WT)寄生虫的IC50值比PfENT1基因敲除(pfent1Δ)寄生虫低至4倍。pfent1Δ寄生虫杀伤表现出WT未观察到的延迟死亡表型。我们推断,在寄生虫中,这些化合物以相似的效力抑制PfENT1和一个次要靶点。次要靶点的身份未知,但其存在可能降低寄生虫对PfENT1抑制剂产生抗性的可能性。我们的数据支持这样的假设,即通过PfENT1阻断嘌呤转运可能是抗疟药物开发的一种新颖且有吸引力的方法。