To investigate the effects and underlying mechanisms of berberine (BBR) on colorectal cancer (CRC) using organoid models.
Approach:
Organoid Models: Established CRC organoid models from KPC transgenic mice and Caco-2 cell line.
Treatment and Evaluation: Treated organoids with different doses of BBR and evaluated morphological characteristics, proliferation, ROS, apoptosis, and cell cycle.
Molecular Mechanisms: Utilized RNA-Seq, epithelial permeability assays, and lipid probes to examine BBR's molecular effects.
Key Findings:
BBR significantly inhibited the growth of KPC and Caco-2 organoids.
BBR decreased the ratio of Ki67 and EdU positive cells in CRC organoids.
BBR increased ROS levels in organoids.
BBR induced cell cycle arrest and disrupted epithelial barrier function.
BBR significantly blocked lipid synthesis in CRC organoids.
Interpretation:
BBR may suppress the malignant phenotype of CRC organoids through mechanisms such as blocking cell cycle progression and disrupting lipid metabolism.
Limitations:
The study primarily focuses on organoid models, which may not fully replicate in vivo conditions and could limit the generalizability of the findings.
Further research is needed to validate findings in clinical settings.
Conclusion:
BBR demonstrates potential as a natural compound for inhibiting CRC growth through various mechanisms.
