Division of Cancer Differentiation, National Cancer Center Research Institute, National Cancer Center, Tokyo, 104-0045, Japan.
Eisai Co., Ltd., Tokyo, 112-8088, Japan.
Biochem Biophys Res Commun. 2022 Jan 1;586:93-99. doi: 10.1016/j.bbrc.2021.11.063. Epub 2021 Nov 19.
Dysregulated activation of the WNT/β-catenin signaling pathway is essential for the initiation and development of various cancers. E7386, a small-molecule compound, attenuates WNT signaling by blocking the interaction between β-catenin and CREB-binding protein (CBP); hence, it is regarded as a therapeutic candidate for cancers with activated WNT signaling. In the present study, we evaluated the biological characteristics associated with E7386 sensitivity by using a panel of patient-derived colon cancer spheroids. An integrative approach that combined E7386 sensitivity and gene expression profiles revealed that the resistance of the cancer spheroids to E7386 was associated with the activation of the NF-κB pathway. NF-κB pathway inhibitors acted synergistically with E7386 to block proliferation and induce cell cycle arrest in E7386-resistant spheroids. These findings suggest a possibility that a combination of E7386 and NF-κB inhibition may effectively block the proliferation of a subset of colon cancer cells.
WNT/β-catenin 信号通路的失调激活对于各种癌症的发生和发展至关重要。E7386 是一种小分子化合物,通过阻断β-catenin 和 CREB 结合蛋白(CBP)之间的相互作用来抑制 WNT 信号,因此被认为是具有激活 WNT 信号的癌症的治疗候选药物。在本研究中,我们使用一组患者来源的结肠癌球体评估了与 E7386 敏感性相关的生物学特征。一种综合方法,将 E7386 敏感性与基因表达谱相结合,表明癌症球体对 E7386 的耐药性与 NF-κB 通路的激活有关。NF-κB 通路抑制剂与 E7386 协同作用,阻断 E7386 耐药球体的增殖并诱导细胞周期停滞。这些发现表明,E7386 和 NF-κB 抑制的联合可能有效地阻断一部分结肠癌细胞的增殖。