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Cell-specific pattern of berberine pleiotropic effects on different human cell lines
Alessandro Agnarelli1, Marco Natali1, Mercedes Garcia-Gil1,2
1Department of Biology, University of Pisa, Pisa, Italy.
Abstract:
The natural alkaloid berberine has several pharmacological properties and recently received attention as a potential anticancer agent. In this work, we investigated the molecular mechanisms underlying the anti-tumor effect of berberine on glioblastoma U343 and pancreatic carcinoma MIA PaCa-2 cells. Human dermal fibroblasts (HDF) were used as non-cancer cells. We show that berberine differentially affects cell viability, displaying a higher cytotoxicity on the two cancer cell lines than on HDF. Berberine also affects cell cycle progression, senescence, caspase-3 activity, autophagy and migration in a cell-specific manner. In particular, in HDF it induces cell cycle arrest in G2 and senescence, but not autophagy; in the U343 cells, berberine leads to cell cycle arrest in G2 and induces both senescence and autophagy; in MIA PaCa-2 cells, the alkaloid induces arrest in G1, senescence, autophagy, it increases caspase-3 activity and impairs migration/invasion. As demonstrated by decreased citrate synthase activity, the three cell lines show mitochondrial dysfunction following berberine exposure. Finally, we observed that berberine modulates the expression profile of genes involved in different pathways of tumorigenesis in a cell line-specific manner. These findings have valuable implications for understanding the complex functional interactions between berberine and specific cell types.
Insights
Berberine exhibits anticancer properties, showing higher toxicity to glioblastoma and pancreatic cancer cells than normal cells. It impacts cell cycle, senescence, and migration differently across cell types, indicating targeted therapeutic potential.
Area of Science:
- Pharmacology
- Molecular Biology
- Cancer Research
Background:
- Berberine, a natural alkaloid, possesses diverse pharmacological activities.
- Emerging evidence suggests berberine's potential as an anticancer agent.
- Understanding its molecular mechanisms is crucial for therapeutic development.
Purpose of the Study:
- To investigate the molecular mechanisms of berberine's anti-tumor effects.
- To compare berberine's impact on glioblastoma, pancreatic carcinoma, and non-cancerous cells.
- To elucidate cell-specific responses to berberine treatment.
Main Methods:
- Cell viability assays on U343 (glioblastoma), MIA PaCa-2 (pancreatic carcinoma), and HDF (fibroblast) cells.
- Analysis of cell cycle progression, senescence, caspase-3 activity, autophagy, and migration.
- Assessment of mitochondrial dysfunction via citrate synthase activity.
- Gene expression profiling to identify modulated tumorigenesis pathways.
Main Results:
- Berberine demonstrated higher cytotoxicity against cancer cells compared to HDF.
- Differential effects on cell cycle (G1/G2 arrest), senescence, autophagy, and migration were observed across cell lines.
- Mitochondrial dysfunction was evident in all cell types following berberine exposure.
- Berberine modulated gene expression profiles related to tumorigenesis in a cell-specific manner.
Conclusions:
- Berberine exhibits differential anti-tumor effects and molecular mechanisms depending on the cell type.
- Its impact on cancer cells involves cell cycle arrest, senescence, autophagy modulation, and impaired migration.
- Mitochondrial dysfunction is a common effect, suggesting a broad cellular stress response.
- These findings highlight berberine's complex interactions with specific cell types, offering insights for targeted cancer therapy.
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