Journal
JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
Volume 36, Issue 7, Pages -Publisher
WILEY
DOI: 10.1002/jbt.23051
Keywords
apoptosis; colon cancer; JNK1; 2; psoralidin; ROS
Categories
Funding
- Science and Technology Development Fund, Macau SAR [0116/2020/A, 0081/2021/A2]
- Shandong Provincial Natural Science Foundation, China [RZ2100002664]
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This study found that Psoralidin (PSO) can induce apoptosis in colon cancer cells through oxidative damage mediated by caspase 3/7 activation and ROS generation.
Psoralidin (PSO) is a natural coumarin isolated from the seeds of Psoralea corylifolia Linn. Previous studies have reported that PSO exerts numerous pharmacological bioactivities including antitumor. The present study aimed to investigate its anticancer effect using colon cancer cells. Cultured HT-29 and HCT-116 colon cancer cells were treated with different concentrations of PSO, and the cell viability, the intracellular reactive oxygen species (ROS), the protein expression, and the apoptosis were determined by MTT assay, DCFH2-DA fluorescence probe, Western blotting, and Annexin V/7-AAD staining, respectively. The activities of caspase 3/7 were determined by a commercial kit. Our study found that PSO effectively induces apoptotic cell death mediated by caspase 3/7 in HT-29 and HCT-116 colon cancer cells. PSO treatment rapidly boosts the ROS generation, which is responsible for the PSO-triggered DNA damage, mitochondria membrane potential decrease and caspase 3/7 activation, and c-Jun N-terminal kinase 1/2 activation. Collectively, these results showed that PSO triggered oxidative damage mediated apoptosis in colon cancer cells.
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