Introduction::The purpose of this research was to settle the role of brucine in pancreatic
ductal adenocarcinoma (PDAC) and the mechanisms involved.
Methods::The findings of this study suggest that brucine exerts inhibitory effects on cell growth,
clonogenicity, and invasive potential of Panc02 and Mia Paca-2 cells. These effects may be linked
to an increase in apoptotic-prone cell population.
Results::Gene sequencing data suggests that these effects are mediated through the induction of
apoptosis. Experimental evidence further supports the notion that brucine reduces mitochondrial
membrane potential and upregulates Bax expression while downregulating Bcl-2 expression. These
effects are believed to be a result of brucine-mediated suppression of PI3K/Akt activity, which
serves as a regulatory factor of mTOR, Bax, and Bcl-2. Suppression of PI3K activity enhances the
tumor-suppressing effects of brucine.
Conclusion::Overall, these findings suggest that brucine has therapeutic potential as a remedy option
for PDAC.