Abstract
BackgroundHouttuynia cordata Thunb (HCT) is commonly used in Taiwan and other Asian countries as an anti-inflammatory, antibacterial and antiviral herbal medicine. In this study, we investigated the anti-human lung cancer activity and growth inhibition mechanisms of HCT in human lung cancer A549 cells.ResultsIn order to investigate effects of HCT on A549 cells, MTT assay was used to evaluate cell viability. Flow cytometry was employed for cell cycle analysis, DAPI staining, and the Comet assay was used for DNA fragmentation and DNA condensation. Western blot analysis was used to analyze cell cycle and apoptotic related protein levels. HCT induced morphological changes including cell shrinkage and rounding. HCT increased the G0/G1 and Sub-G1 cell (apoptosis) populations and HCT increased DNA fragmentation and DNA condensation as revealed by DAPI staining and the Comet assay. HCT induced activation of caspase-8 and caspase-3. Fas/CD95 protein levels were increased in HCT-treated A549 cells. The G0/G1 phase and apoptotic related protein levels of cyclin D1, cyclin A, CDK 4 and CDK 2 were decreased, and p27, caspase-8 and caspase-3 were increased in A549 cells after HCT treatment.ConclusionsThe results demonstrated that HCT-induced G0/G1 phase arrest and Fas/CD95-dependent apoptotic cell death in A549 cells
Highlights
Houttuynia cordata Thunb (HCT) is commonly used in Taiwan and other Asian countries as an antiinflammatory, antibacterial and antiviral herbal medicine
Effect of HCT on viability of A549 cells Cell viability of HCT (0, 125, 250 and 500 μg/ml) treated A549 cells was determined by MTT assay for 24 and 48 h
Effect of HCT on cell-cycle distribution and apoptosis in A549 cells To evaluate the effects of HCT on cell-cycle distribution and apoptosis, A549 cells were treated with HCT (0, 125, 250 and 500 μg/ml)
Summary
Houttuynia cordata Thunb (HCT) is commonly used in Taiwan and other Asian countries as an antiinflammatory, antibacterial and antiviral herbal medicine. Radiotherapy, and chemo-therapy are used for treating lung cancer patients [1,2,3]. Induction of cell cycle arrest and/or apoptosis in lung cancer cells has been considered an influential treatment strategy [4,5,6]. Previous studies have demonstrated that the cell membrane death receptor played an important role in apoptosis [11,12]. The activation of caspase-3 by caspase-8 is responsible for the cleavage of cellular substrates [13,14,15,16,17,18,19,20]. Cleavage of cellular substrates degrades the chromosomes into fragments during apoptosis [13,14,15,16,21]
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