Comprehensive Summary
In order to better understand how Berberine (BBR) exhibits anti-colorectal cancer (CRC) activity, this study investigated the ferroptosis signaling pathway to see if BBR influences disordered mitochondrial energy metabolism in CRC cells. The study performed both in vivo and in vitro cell effects of BBR on malignant phenotypes. Using CRC cell lines HCT116 and CT26, the study found that BBR inhibited CRC cell proliferation and increased ferroptosis markers while also suppressing ATP levels and other metabolism-related enzymes. Using a convolutional network-based drug pathway algorithm, Gli1 was predicted as a target for binding. This prediction was confirmed and the study found that BBR performed its anti-CRC activity by inhibiting the Gli1/STAT3-ferroptosis negative regulation axis. On top of this, BBR showed no significant toxicity in vivo. Overall, this study identified a novel pathway for BBR’s anti-CRC activity, supporting new medical interventions to reduce cancer in vivo.
Outcomes and Implications
The findings of this study have important implications for healthcare and oncology practice. The study revealed that BBR induces ferroptosis and disrupts energy metabolism in CRC cells by inhibiting Gli1/STAT3-FNR axis, highlighting a potential novel therapeutic strategy for CRC treatment. Health-care providers may consider incorporating BBR or chemically similar compounds alongside traditional treatment methods in resolving CRC on a patient basis. Future research in this topic may help health-care professionals identify and employ new treatment biomarkers and personalize cancer therapy, ultimately improving patient outcomes.