Crocin Suppresses Colorectal Cancer Cell Proliferation by Regulating miR-143/145 and KRAS/RREB1 Pathways

Background As a chemoprevention agent, crocin effectively decreases the risk of human cancers, including colorectal cancer (CRC). However, the mechanism underlying the anti-cancer effects of crocin is not entirely explained. Considering that in this study, we investigated the crocin effect on miR-143/145 and related signaling pathways in CRC cells.Methods HCT-116 and HT-29 CRC cells were treated with different concentrations of crocin and then were subjected to MTT and qRT-PCR assays to investigate cell viability and miR-143/miR-145, KRAS, and RREB1 expression, respectively. Also, western blotting was performed to evaluate gene expression at protein levels.Results Our results showed that treating CRC cells with crocin decreases cell viability by upregulating miR-143/145 expression and reducing KRAS and RREB1 expression dose-dependently. These effects on gene expression in CRC cells were reversed by removing crocin from the media after 48 h. Furthermore, western blotting results exhibited that crocin significantly reduced the protein expression of KRAS and RREB1. Also, it was found that treatment of CRC cells by crocin led to the inactivation of AKT by decreasing its phosphorylation.Conclusion This study suggests that crocin may inhibit CRC cell proliferation by modulating KRAS, REEB1, and AKT signaling pathways mediated through miR-143/145 upregulation.

Automated summary

The study showed that crocin decreases cell viability in colorectal cancer cells by upregulating miR-143/145 expression and decreasing KRAS and RREB1 expression dose-dependently. Furthermore, crocin treatment also led to the inactivation of AKT by decreasing its phosphorylation, suggesting a potential inhibitory effect on CRC cell proliferation.