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.
Highlights
Colorectal cancer (CRC) is a major cause of tumor-related deaths because of its spreading capability and metastatic characteristic [1, 2]
We provided the first evidence supporting that Licochalcone A (LCA) stimulated reactive oxygen species (ROS) production in HCT-116 cells, in turn promoting G0/G1 phase arrest
This was demonstrated by the low expression of CDC2, a cyclin-dependent kinase, whose inhibition leads to G0/G1 phase arrest [10]
Summary
Colorectal cancer (CRC) is a major cause of tumor-related deaths because of its spreading capability and metastatic characteristic [1, 2]. Traditional chemotherapeutic drugs such as 5-fluorouracil and cisplatin are often limited by drug resistance and side effects. Natural products and their analogs are promising anticancer drugs because of their remarkable effects, low toxicity, and reduced side effects. Accumulating evidence has demonstrated that LCA exhibited anticancer activity through modulating reactive oxygen species (ROS) levels in cancer cells. Hao et al suggested that LCA enhanced BGC823 human gastric cancer cell apoptosis by activating ROSmediated mitogen-activated protein kinase and PI3K/AKT signaling pathways [6]. Previous research has demonstrated that LCA attenuated the expression of inflammatory mediators, in turn modifying the tumor microenvironment and suppressing CRC formation and progression [8]. Whether LCA mediates the progression of CRC by regulating ROS production and the underlying targets remains unclear
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