Ginseng bioactive compounds reverse rectal cancer therapy resistance by targeting CYP26A1 and modulating B-Cell mediated immunity

This study explores how ginseng bioactive compounds overcome radio- and chemoresistance in rectal cancer by targeting CYP26A1 and modulating immunity. Bioinformatic analyses identified CYP26A1 as a critical resistance-related gene associated with poor prognosis and reduced B-cell infiltration. Molecular docking revealed strong binding between CYP26A1 and five ginseng components (Aposiopolamine, Celabenzine, Frutinone A, Girinimbin, and Inermin). In vitro experiments further confirmed that ginseng extract inhibited the proliferation of colorectal cancer cells, induced apoptosis, caused cell-cycle arrest, and suppressed cell migration and invasion. In addition, ginseng extract enhanced B-cell activity and promoted the secretion of granzyme B, IFN-γ, and TNF-α, thereby modulating the immune microenvironment and ultimately influencing tumor cell sensitivity to radiotherapy and chemotherapy. Collectively, these findings suggest that ginseng bioactives may reverse treatment resistance through CYP26A1 inhibition and immune modulation, highlighting their potential as adjuvants to improve therapeutic response in rectal cancer.