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

Licochalcone A (LCA) exhibited anticancer activity through modulating reactive oxygen species 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 production remains unclear. To address this, HCT-116 cells were treated with LCA, resulting in G0/G1 phase arrest, apoptosis, and high duanyu1670 generation, which were attenuated by N-acetyl-L-cysteine, a duanyu1670 inhibitor. In addition, LCA suppressed the expression of thioredoxin reductase 1 (TrxR1) in HCT-116 cells, leading to high duanyu1670 levels and apoptosis. Moreover, LCA administration combined with TrxR1 inhibition further enhanced the production of duanyu1670 and apoptosis in HCT-116 cells compared to LCA administration or TrxR1 inhibition alone. These results demonstrated that LCA might enhance the production of duanyu1670 by targeting TrxR1, leading to apoptosis in HCT-116 cells, which provides potential insight for the interventional treatment of CRC.

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