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In the gastric cancer cells SNU-5, BBR induced the production of Reactive Oxygen Species (ROS) while decreasing the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). In pancreatic cancer cells, BBR treatment also influenced citrate metabolism resulting in blocking of the fatty acid biosynthesis. Based on a phenotypic assay, berberine showed a notable inhibitory role in pancreatic cancer cell metastasis and viability. BBR showed inhibitory effects in pancreatic cancer cells (PANC-1, AsPC-1, and MIA-PaCa-2) on the expression of Rad51 and the upregulation of PARP expression compared with control pancreatic cancer cells. Table 2 highlights the effect of berberine against various pancreatic cancer cell lines along with its proposed mechanisms of action. Therefore, the outcomes of that study concluded that combined treatment with berberines and NAX compounds may help suppress the proliferation of pancreatic cancer cells . In contrast, induction of apoptosis was triggered by a mechanism involving the production of reactive oxygen species (ROS) rather than activation of caspase 3/7. In the pancreatic cancer cell lines PANC-1 and MIA-PaCa2, Park et al. identified the anticancer role of berberine via a variety of pathways such as induction of phase G1. Similar results were obtained with metformin used at doses that produced either a moderate or significant decrease in intracellular ATP levels, almost identical to the decrease in ATP levels observed in response to BBR . BBR lowers mitochondrial membrane potential and intracellular ATP levels and induces potent AMPK activation, as evidenced by phosphorylation of the AMPK α subunit at Thr172 and acetyl CoA carboxylase (ACC) at Ser79. Table 2 provides an overview of berberine action against various colon cancer cell lines and the proposed anticancer mechanisms. 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