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新型IκB激酶β抑制剂IMD-0560在卵巢癌异种移植模型小鼠中具有强大的治疗效果。

The Novel IκB Kinase β Inhibitor, IMD-0560, Has Potent Therapeutic Efficacy in Ovarian Cancer Xenograft Model Mice.

作者信息

Sawada Ikuko, Hashimoto Kae, Sawada Kenjiro, Kinose Yasuto, Nakamura Koji, Toda Aska, Nakatsuka Erika, Yoshimura Akihiko, Mabuchi Seiji, Fujikawa Tomoyuki, Itai Akiko, Kimura Tadashi

机构信息

*Department of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, Osaka; and †Institute of Medicinal Molecular Design, Inc, Bunkyo-ku, Tokyo, Japan.

出版信息

Int J Gynecol Cancer. 2016 May;26(4):610-8. doi: 10.1097/IGC.0000000000000668.

Abstract

OBJECTIVE

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.

METHODS

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.

RESULTS

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.

CONCLUSIONS

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.

摘要

目的

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。

方法

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。

结果

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。

结论

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。

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