Sawada Ikuko, Hashimoto Kae, Sawada Kenjiro, Kinose Yasuto, Nakamura Koji, Toda Aska, Nakatsuka Erika, Yoshimura Akihiko, Mabuchi Seiji, Fujikawa Tomoyuki, Itai Akiko, Kimura Tadashi
*Department of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka; and †Institute of Medicinal Molecular Design, Inc, Bunkyo-ku, Tokyo, Japan.
Int J Gynecol Cancer. 2016 May;26(4):610-8. doi: 10.1097/IGC.0000000000000668.
Aberrant activation of nuclear factor-kappa β (NF-κB) signaling has been correlated with poor outcome among patients with ovarian cancer. Although the therapeutic potential of NF-κB pathway disruption in cancers has been extensively studied, most classical NF-κB inhibitors are poorly selective, exhibit off-target effects, and have failed to be applied in clinical use. IMD-0560, N-[2,5-bis (trifluoromethyl) phenyl]-5-bromo-2-hydroxybenzamide, is a novel low-molecular-weight compound that selectively inhibits the IκB kinase complex and works as an inhibitor of NF-κB signaling. The aim of this study was to assess the therapeutic potential of IMD-0560 against ovarian cancer in vitro and in vivo.
NF-κB activity (phosphorylation) was determined in 9 ovarian cancer cell lines and the inhibitory effect of IMD-0560 on NF-κB activation was analyzed by Western blotting. Cell viability, cell cycle, vascular endothelial growth factor (VEGF) expression, and angiogenesis were assessed in vitro to evaluate the effect of IMD-0560 on ovarian cancer cells. In vivo efficacy of IMD-0560 was also investigated using an ovarian cancer xenograft mouse model.
The NF-κB signaling pathway was constitutively activated in 8 of 9 ovarian cancer cell lines. IMD-0560 inhibited NF-κB activation and suppressed ovarian cancer cell proliferation by inducing G1 phase arrest. IMD-0560 decreased VEGF secretion from cancer cells and inhibited the tube formation of human umbilical vein endothelial cells. IMD-0560 significantly inhibited peritoneal metastasis and prolonged the survival in an ovarian cancer xenograft mice model. Immunohistochemical staining of excised tumors revealed that IMD-0560 suppressed VEGF expression, tumor angiogenesis, and cancer cell proliferation.
IMD-0560 showed promising therapeutic efficacy against ovarian cancer xenograft mice by inducing cell cycle arrest and suppressing VEGF production from cancer cells. IMD-0560 may be a potential future option in regimens for the treatment of ovarian cancer.
核因子-κB(NF-κB)信号通路的异常激活与卵巢癌患者的不良预后相关。尽管癌症中NF-κB信号通路阻断的治疗潜力已得到广泛研究,但大多数经典的NF-κB抑制剂选择性较差,具有脱靶效应,且未能应用于临床。IMD-0560,即N-[2,5-双(三氟甲基)苯基]-5-溴-2-羟基苯甲酰胺,是一种新型低分子量化合物,可选择性抑制IκB激酶复合物,并作为NF-κB信号通路的抑制剂发挥作用。本研究的目的是评估IMD-0560在体外和体内对卵巢癌的治疗潜力。
在9种卵巢癌细胞系中测定NF-κB活性(磷酸化水平),并通过蛋白质免疫印迹法分析IMD-0560对NF-κB激活的抑制作用。在体外评估细胞活力、细胞周期、血管内皮生长因子(VEGF)表达和血管生成,以评价IMD-0560对卵巢癌细胞的作用。还使用卵巢癌异种移植小鼠模型研究了IMD-0560的体内疗效。
9种卵巢癌细胞系中有8种的NF-κB信号通路呈组成性激活。IMD-0560通过诱导G1期阻滞抑制NF-κB激活并抑制卵巢癌细胞增殖。IMD-0560减少癌细胞分泌VEGF,并抑制人脐静脉内皮细胞的管腔形成。IMD-0显著抑制卵巢癌异种移植小鼠模型中的腹膜转移并延长生存期。对切除肿瘤的免疫组织化学染色显示,IMD-0560抑制VEGF表达、肿瘤血管生成和癌细胞增殖。
IMD-0560通过诱导细胞周期阻滞和抑制癌细胞产生VEGF,对卵巢癌异种移植小鼠显示出有前景的治疗效果。IMD-0560可能是未来卵巢癌治疗方案中的一个潜在选择。