LZ-106, a novel analog of enoxacin, inducing apoptosis via activation of ROS-dependent DNA damage response in NSCLCs

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LZ-106, a novel analog of enoxacin, inducing apoptosis via activation of ROS-dependent DNA damage response in NSCLCs

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作者：Lin Yang^a ; ¹ ; Yinan Yuan^a ; ¹ ; Chengyu Fu^a ; Xuefen Xu^a ; Jieying Zhou^a ; Shuhao Wang^a ; Lingyi Kong^b ; Zhiyu Li^a ; Qinglong Guo^a ; ^{anticancer_drug@163.com" class="auth_mail" title="E-mail the corresponding author} ; Libin Wei^a ; ^{wlbiws_1986@aliyun.com" class="auth_mail" title="E-mail the corresponding author}
关键词：Quinolone ; NSCLC ; ROS ; DDR ; Apoptosis
刊名：Free Radical Biology and Medicine
出版年：2016
出版时间：June 2016
年：2016
卷：95
期：Complete
页码：155-168
全文大小：7912 K

文摘

•: LZ-106, a derivative of quinolones, exhibits antitumor and apoptosis induction effects in vitro and in vivo.
•: Both mitochondrial and ER-stress apoptosis pathway are activated by LZ-106.
•: ROS serves as a major cause in mechanism of action of LZ-106 by triggering ROS-dependent DNA damage response.
•: The main type of ROS caused by LZ-106 is superoxide anions.

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