作者: Naomasa Ishida , Takuya Fukazawa , Yutaka Maeda , Tomoki Yamatsuji , Katsuya Kato
DOI: 10.1016/J.YEXCR.2015.03.019
关键词:
摘要: The PI3K–AKT pathway is expected to be a therapeutic target for non-small cell lung cancer (NSCLC) treatment. We previously reported that novel PI3K inhibitor iMDK suppressed NSCLC cells in vitro and vivo without harming normal mice. Unexpectedly, activated the MAPK pathway, including ERK, cells. Since did not eradicate such completely, it possible confers resistance against death induced by iMDK. In present study, we assessed whether suppressing of iMDK-mediated activation would enhance anti-tumorigenic activity PD0325901, inhibitor, cooperatively inhibited viability colony formation inducing apoptosis vitro. HUVEC tube formation, representing angiogenic processes vitro, was also combinatorial treatment PD0325901. with PD0325901 tumor growth tumor-associated angiogenesis xenograft model vivo. Here, demonstrate strategy using NSCLC.