Chlorogenic acid (CGA) is one of the polyphenols identified in the human diet. Previous studies have shown that CGA plays a protective role against liver diseases. The colon plays a pivotal role in CGA metabolism. However, little is known about the direct effects and the underlying molecular mechanisms of CGA in colon cancer. Here, we investigate these mechanisms of CGA activity in human colon cancer cells. The effects of CGA on the viability of two human colon cancer cell lines, HCT116 and HT29, were determined using the MTT assay. The intracellular reactive oxygen species (ROS) were detected using fluorescence microscopy and flow cytometry. In addition, changes in cell proliferation were detected by cell cycle analysis. Immunoblotting analysis was used to observe the underlying molecular changes. CGA inhibited the viability of HCT116 and HT29 cells in a dose-dependent manner. CGA induced ROS production, whereas the combined use of ROS scavenger N-acetylcysteine attenuated the CGA-induced viability inhibition. Moreover, CGA induced cell cycle arrest at the S phase and suppressed the activation of extracellular signal-related kinase in both cell types, which likely contributes toward the ROS-induced viability inhibition caused by CGA treatment. CGA-induced ROS production inhibited cell viability in human colon cancer cells. CGA caused S-phase arrest and extracellular signal-related kinase inactivation that may have led to the observed viability inhibition. CGA is therefore a potential treatment against CRC. Copyright (C) 2016 Wolters Kluwer Health, Inc. All rights reserved.
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