https://www.selleckchem.com/products/gdc6036.html
In addition, treatment of PL caused DNA damage in a dose-dependent manner. PL arrested the cell cycle at S-G2/M phase, and enhanced reactive oxygen species (ROS) generation. Excess ROS generated by PL disrupted mitochondrial membrane resulted in depletion of mitochondrial membrane potential (MMP). These results conclude that PL decreases lung cancer cell viability by arresting cells at S-G2/M phase, and induces apoptosis by activation of mitochondrial-mediated apoptotic pathway through excess ROS generation. Overall findings suggest tha
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