自噬
拉沙酸
活性氧
细胞凋亡
癌细胞
细胞生物学
化学
程序性细胞死亡
生物化学
癌症研究
生物
癌症
膜
遗传学
离子载体
作者
Kwang-Youn Kim,Sanghun Kim,Sun-Nyoung Yu,Sul-Gi Park,Young-Wook Kim,Hyo-Won Nam,Hyun-Hee An,Hak Sun Yu,Young Ho Kim,Jae-Hoon Ji,Young Joon Seo,Soon-Cheol Ahn
标识
DOI:10.1016/j.biopha.2017.01.140
摘要
Lasalocid is an antibiotic from the group of carboxylic ionophores, produced by Streptomyces lasaliensis. But there was limited information of lasalocid on human prostate cancer cells. In the present studies, to better understand its effect in human prostate cancer cells, apoptosis and autophagy associated with possible signal pathways in vitro was examined. Our study showed that lasalocid mediated cell cycle arrest in G0/G1 phase by reducing G1 phase dependent proteins, indicating entering into apoptotic cell death pathway. Lasalocid-induced apoptosis was involved with reactive oxygen species (ROS) production, and mitochondrial hyperpolarization. In addition, lasalocid induced autophagy through microtubule-associated protein 1 light chain 3 (LC-3)-II conversion, acidic vesicular organelles formation and GFP-LC-3 punctuate, which was inhibited by 3-methyladenine (3-MA), a widely used pharmacological inhibitor of autophagy. Furthermore, the autophagic phenomena were mediated by production of ROS, confirming that inhibition of ROS with N-acetyl-l-cysteine, a ROS inhibitor, attenuated lasalocid-triggered autophagy. Inhibition of autophagy with 3-MA enhanced the lasalocid-induced apoptosis through enhanced ROS generation. Taken together, lasalocid should be useful in the search for new potential chemotherapeutic agents for understanding the molecular mechanisms of anticancer in prostate cancer cells.
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