期刊
ANTICANCER RESEARCH
卷 41, 期 12, 页码 5935-5944出版社
INT INST ANTICANCER RESEARCH
DOI: 10.21873/anticanres.15412
关键词
Capsicodendrin; MCF-7; NF-kappa B; IKK beta; ICAM-1; ROS; caspase-7; caspase-1
类别
资金
- National Cancer Institute, NIH, Bethesda, MD [P01 CA125066, P01 CA125066-10S1]
- Jack L. Beal Endowment Fund
Capsicodendrin demonstrated potential anticancer effects in MCF-7 cancer cells by increasing ROS levels to promote caspase-1 activity and induce cell death, suggesting it may be a promising agent for preventing the progression of metastatic breast cancer.
Background/Aim: Effect of capsicodendrin on the NF-KB pathway was studied in MCF-7 cancer cells. Materials and Methods: The transcription factor assay was used to screen for NF-KB activity. The effect on IKK beta, ICAM-1, and caspase-7 were studied using western blot. Caspase-1 was studied using Promega Caspase-Glo (R) assay. Reactive oxygen species (ROS) were detected using the fluorescent probe DCFH-DA. The potentiometric dye JC-1 was used to assess mitochondrial membrane potential (Delta psi m) and the cell cycle was examined using a fluorescence-activated cell sorter. Results: NF-kappa B p65 inhibitory effect was IC50=8.6 mu M and cytotoxic activity was IC50=7.5 mu M. The upstream IKK and the downstream ICAM-1 were down-regulated. Sub G1-phase population increased to 81% after 12 h of treatment with capsicodendrin (10 mu M) and there was no loss of Delta psi M. Conclusion: Increased levels of intracellular ROS promoted activity of caspase-1 and induced cell death in MCF-7 cells. Capsicodendrin may be a future anticancer agent that prevents the progression of metastatic breast cancer.
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