Calystegia soldanella extract induces apoptosis in HCT116 cells by disrupting calcium ion homeostasis and promoting reactive oxygen species generation

초록

BackgroundColorectal cancer (CRC) has a high global incidence and mortality rate. Modern CRC treatment is largely limited due to its high recurrence rate, as well as treatment toxicity and drug resistance. Against this background, phytochemicals are attracting attention as promising candidates for cancer treatment due to their low toxicity levels and various pharmacological activities. Calystegia soldanella, a halophyte native to the Korean coastline, has been reported to exert antioxidant and anticancer effects, but the underlying molecular mechanisms remain unclear.ObjectivesIn this study, we investigated the antioxidant and anticancer effects of C. soldanella extracts on the viability of the CRC cell line HCT116.ResultsCalystegia soldanella extracts collected from Myeonjeon-ri significantly reduced HCT116 cell viability (IC50: 9.614 & micro;g/mL). In contrast, C. soldanella extracts collected from Hanmun-ri did not reach the IC50 value within the tested concentration range. Both C. soldanella extracts disrupted Ca2+ homeostasis by increasing cytosol and mitochondrial Ca2+ accumulation, promoting reactive oxygen species (ROS) production, and significantly upregulating inflammation-related genes, including IL13, IL18, IL18R1, IL21, and CXCL1. These results suggest that C. soldanella induces apoptosis in HCT116 cells by dysregulating Ca2+ homeostasis and increasing ROS-mediated stress, while simultaneously activating apoptosis and inflammatory signaling pathways. Moreover, regional differences in C. soldanella activity against HCT116 cells demonstrate the importance of the growth environment in forming metabolites or bioactive compounds in plants.ConclusionCollectively, our study findings reveal the molecular biological mechanisms of C. soldanella, suggesting its potential as a candidate or therapeutic adjuvant for CRC treatment.

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