Elayapillai Sugantha Priya, Gandhi Anjalika, Dogra Samrita, Saunders Debra, Smith Nataliya, Hladik Cole, Towner Rheal A, Moxley Katherine M, Hannafon Bethany N
Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma.
Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma.
J Pharmacol Exp Ther. 2025 Jan;392(1):100004. doi: 10.1124/jpet.124.002223. Epub 2024 Nov 22.
Advanced-stage endometrial cancer patients typically receive a combination of platinum and paclitaxel chemotherapy. However, limited treatment options are available for those with recurrent disease, and there is a need to identify alternative treatment options for the advanced setting. Our goal was to evaluate the preclinical efficacy and mechanism of action of the anticancer drug Oklahoma Nitrone-007 (OKN-007) alone and in combination with carboplatin and paclitaxel in endometrial cancer. The effect of OKN-007 on the metabolic viability of endometrial cancer cells in both two- and three-dimensional (2D and 3D) cultures, as well as on clonogenic growth, in vitro was assessed. We also evaluated OKN-007 in vivo using an intraperitoneal xenograft model and targeted gene expression profiling to determine the molecular mechanism and gene expression programs altered by OKN-007. Our results showed that endometrial cancer cells were generally sensitive to OKN-007 in both 2D and 3D cultures. OKN-007 displayed a reduction in 3D spheroid and clonogenic growth. Subsequent targeted gene expression profiling revealed that OKN-007 significantly downregulated the immunosuppressive immunometabolic regulatory enzyme indolamine 2,3-dioxygenase 1 (IDO1) (-11.27-fold change) and modulated upstream inflammatory pathways that regulate IDO1 expression (interferon-gamma [IFN-γ], Janus kinase/signal transducer and activator of transcription [JAK-STAT], transforming growth factor beta [TGF-β], and nuclear factor-kappa B [NF-κB]), downstream IDO1 effector pathways (mammalian target of rapamycin [mTOR] and aryl hydrocarbon receptor [AhR]), and altered T cell signaling pathways. OKN-007 treatment reduced IDO1, sulfatase 2 (SULF2), and TGF-β protein expression in vivo and inhibited TGF-β, NF-κB, and AhR-mediated nuclear signaling in vitro. These findings indicate that OKN-007 surmounts proinflammatory, immunosuppressive, and protumorigenic pathways and is a promising approach for the effective treatment of endometrial cancer. SIGNIFICANCE STATEMENT: Women with advanced and recurrent endometrial cancer have limited therapeutic options. Oklahoma Nitrone-007 (OKN-007), which has minimal toxicity and is currently being evaluated in early-phase clinical trials for the treatment of cancer, is a potential new strategy for the treatment of endometrial cancer.
晚期子宫内膜癌患者通常接受铂类和紫杉醇联合化疗。然而,对于复发患者,可用的治疗选择有限,因此需要为晚期患者确定替代治疗方案。我们的目标是评估抗癌药物俄克拉荷马硝酮-007(OKN-007)单独以及与卡铂和紫杉醇联合使用时在子宫内膜癌中的临床前疗效和作用机制。评估了OKN-007对二维和三维(2D和3D)培养的子宫内膜癌细胞代谢活力以及体外克隆形成生长的影响。我们还使用腹腔内异种移植模型在体内评估了OKN-007,并通过靶向基因表达谱分析来确定由OKN-007改变的分子机制和基因表达程序。我们的结果表明,子宫内膜癌细胞在2D和3D培养中通常对OKN-007敏感。OKN-007使3D球体和克隆形成生长减少。随后的靶向基因表达谱分析显示,OKN-007显著下调免疫抑制性免疫代谢调节酶吲哚胺2,3-双加氧酶1(IDO1)(变化倍数为-11.27倍),并调节调节IDO1表达的上游炎症途径(干扰素-γ[IFN-γ]、Janus激酶/信号转导和转录激活因子[JAK-STAT]、转化生长因子β[TGF-β]和核因子-κB[NF-κB])、IDO1下游效应途径(雷帕霉素靶蛋白[mTOR]和芳烃受体[AhR]),并改变T细胞信号通路。OKN-007治疗降低了体内IDO1、硫酸酯酶2(SULF2)和TGF-β蛋白表达,并在体外抑制了TGF-β、NF-κB和AhR介导的核信号传导。这些发现表明,OKN-007克服了促炎、免疫抑制和促肿瘤途径,是有效治疗子宫内膜癌的一种有前景的方法。意义声明:晚期和复发性子宫内膜癌女性的治疗选择有限。俄克拉荷马硝酮-007(OKN-007)毒性极小,目前正在进行癌症治疗的早期临床试验评估,是治疗子宫内膜癌的一种潜在新策略。