Licochalcone a Induces ROS-Mediated Apoptosis through TrxR1 Inactivation in Colorectal Cancer Cells

Abstract

Licochalcone A (LCA) exhibited anticancer activity through modulating reactive oxygen species (ROS) levels in some cancer cells and has been evidenced to suppress colorectal cancer (CRC) formation and progression. However, whether LCA mediates the progression of CRC by regulating ROS production remains unclear. To address this, HCT-116 cells were treated with LCA, resulting in G0/G1 phase arrest, apoptosis, and high ROS generation, which were attenuated by N-acetyl-L-cysteine, a ROS inhibitor. In addition, LCA suppressed the expression of thioredoxin reductase 1 (TrxR1) in HCT-116 cells, leading to high ROS levels and apoptosis. Moreover, LCA administration combined with TrxR1 inhibition further enhanced the production of ROS and apoptosis in HCT-116 cells compared to LCA administration or TrxR1 inhibition alone. These results demonstrated that LCA might enhance the production of ROS by targeting TrxR1, leading to apoptosis in HCT-116 cells, which provides potential insight for the interventional treatment of CRC.