Dave Nimita, Chow Lionel M L, Gudelsky Gary A, LaSance Kathleen, Qi Xiaoyang, Desai Pankaj B
The James L. Winkle College of Pharmacy, University of Cincinnati, Cincinnati, Ohio.
Cancer and Blood Disease Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Mol Cancer Ther. 2015 Apr;14(4):857-64. doi: 10.1158/1535-7163.MCT-14-0743. Epub 2015 Feb 18.
We present data that letrozole, an extensively used aromatase inhibitor in the treatment of estrogen receptor-positive breast tumors in postmenopausal women, may be potentially used in the treatment of glioblastomas. First, we measured the in vitro cytotoxicity of letrozole and aromatase (CYP19A1) expression and activity in human LN229, T98G, U373MG, U251MG, and U87MG, and rat C6 glioma cell lines. Estrogen receptor (ER)-positive MCF-7 and ER-negative MDA-MB-231 cells served as controls. Cytotoxicity was determined employing the MTT assay, and aromatase activity using an immunoassay that measures the conversion of testosterone to estrogen. Second, in vivo activity of letrozole was assessed in Sprague-Dawley rats orthotopically implanted with C6 gliomas. The changes in tumor volume with letrozole treatment (4 mg/kg/day) were assessed employing μPET/CT imaging, employing [(18)F]-fluorodeoxyglucose (F18-FDG) as the radiotracer. Brain tissues were collected for histologic evaluations. All glioma cell lines included here expressed CYP19A1 and letrozole exerted considerable cytotoxicity and decrease in aromatase activity against these cells (IC50, 0.1-3.5 μmol/L). Imaging analysis employing F18-FDG μPET/CT demonstrated a marked reduction of active tumor volume (>75%) after 8 days of letrozole treatment. Immunohistochemical analysis revealed marked reduction in aromatase expression in tumoral regions of the brain after letrozole treatment. Thus, employing multifaceted tools, we demonstrate that aromatase may be a novel target for the treatment of gliomas and that letrozole, an FDA-approved drug with an outstanding record of safety may be repurposed for the treatment of such primary brain tumors, which currently have few therapeutic options.
我们提供的数据表明,来曲唑这种在绝经后女性雌激素受体阳性乳腺肿瘤治疗中广泛使用的芳香化酶抑制剂,可能有潜力用于治疗胶质母细胞瘤。首先,我们测定了来曲唑在人LN229、T98G、U373MG、U251MG和U87MG以及大鼠C6胶质瘤细胞系中的体外细胞毒性、芳香化酶(CYP19A1)表达和活性。雌激素受体(ER)阳性的MCF-7细胞和ER阴性的MDA-MB-231细胞作为对照。采用MTT法测定细胞毒性,使用测量睾酮向雌激素转化的免疫分析法测定芳香化酶活性。其次,在原位植入C6胶质瘤的Sprague-Dawley大鼠中评估来曲唑的体内活性。采用μPET/CT成像,以[(18)F] - 氟脱氧葡萄糖(F18-FDG)作为放射性示踪剂,评估来曲唑治疗(4mg/kg/天)后肿瘤体积的变化。收集脑组织进行组织学评估。这里纳入的所有胶质瘤细胞系均表达CYP19A1,来曲唑对这些细胞具有相当大的细胞毒性并降低芳香化酶活性(IC50,0.1 - 3.5μmol/L)。使用F18-FDG μPET/CT进行的成像分析表明,来曲唑治疗8天后活性肿瘤体积显著减少(>75%)。免疫组织化学分析显示,来曲唑治疗后大脑肿瘤区域的芳香化酶表达显著降低。因此,通过多方面的工具,我们证明芳香化酶可能是治疗胶质瘤的一个新靶点,而来曲唑这种具有出色安全记录的FDA批准药物可能被重新用于治疗此类原发性脑肿瘤,目前此类肿瘤的治疗选择很少。