Department of Pathology, College of Medicine, Hanyang University, Seoul, Korea.
Cancer Sci. 2011 Mar;102(3):597-604. doi: 10.1111/j.1349-7006.2010.01817.x. Epub 2011 Jan 10.
Epidermal growth factor receptor (EGFR) is one of the most promising targets for cancer therapy. Here, we show the in vitro and in vivo anticancer effects and associated mechanisms of KO-202125, one of the synthesized aristolactam analogs, as a novel EGFR inhibitor, in EGFR-overexpressing cancer cell lines. KO-202125 showed more effective growth inhibition and apoptosis induction than gefitinib, a representative EGFR inhibitor, in various EGFR-overexpressing human cancers including estrogen receptor (ER)-negative MDA-MB-231 human breast cancer cells. Epidermal growth factor receptor phosphorylation at Tyr1068 was reduced and, consequently, the association of EGFR with p85 was decreased by KO-202125 treatment in MDA-MB-231 cell lines. This led to inactivation of the PI3K/Akt pathway, and consequently suppression of activation of the Wnt pathway and enhancement of the nuclear import of p27Kip1. KO-202125 treatment in nude mice injected with MDA-MB-231 cells showed inhibition of tumor growth without toxicity. Collectively, our results showed the possibility of KO-202125 as an effective therapy agent of EGFR-overexpressing cancer cells through reduced EGFR activity and downregulation of the Akt pathway.
表皮生长因子受体(EGFR)是癌症治疗最有前途的靶点之一。在这里,我们展示了 KO-202125 的体外和体内抗癌作用及其相关机制,KO-202125 是一种合成的马兜铃内酰胺类似物,作为一种新型的 EGFR 抑制剂,在 EGFR 过表达的癌细胞系中。与代表性的 EGFR 抑制剂吉非替尼相比,KO-202125 在各种 EGFR 过表达的人类癌症中(包括雌激素受体(ER)阴性的 MDA-MB-231 人乳腺癌细胞)显示出更有效的生长抑制和凋亡诱导作用。在 MDA-MB-231 细胞系中,KO-202125 处理后,EGFR 的 Tyr1068 磷酸化减少,因此与 p85 的结合减少。这导致 PI3K/Akt 通路失活,进而抑制 Wnt 通路的激活和核内 p27Kip1 的导入。在注射 MDA-MB-231 细胞的裸鼠中,KO-202125 治疗显示出抑制肿瘤生长而无毒性。总之,我们的结果表明,KO-202125 通过降低 EGFR 活性和下调 Akt 通路,有可能成为 EGFR 过表达癌细胞的有效治疗剂。