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Okadaic acid toxin at sublethal dose produced cell proliferation in gastric and colon epithelial cell lines
Miguel del Campo1, Héctor Toledo, Néstor Lagos
1Laboratory of Membrane Biochemistry, Program of Physiology and Biophysics, Faculty of Medicine, University of Chile, Independencia 1027, Correo 7, Santiago 8380000, Chile. nlagos@med.uchile.cl.
Abstract:
The aim of this study was to analyze the effect of Okadaic Acid (OA) on the proliferation of gastric and colon epithelial cells, the main target tissues of the toxin. We hypothesized that OA, at sublethal doses, activates multiple signaling pathways, such as Erk and Akt, through the inhibition of PP2A. To demonstrate this, we carried out curves of doses and time response against OA in AGS, MKN-45 and Caco 2 cell lines, and found an increase in the cell proliferation at sublethal doses, at 24 h or 48 h exposure. Indeed, cells can withstand high concentrations of the toxin at 4 h exposure, the time chosen considering the maximum time before total gastric emptying. We have proved that this increased proliferation is due to an overexpression of Cyclin B, a cyclin that promotes the passage from G2 to mitosis. In addition, we have demonstrated that OA induces activation of Akt and Erk in the three cells lines, showing that OA can activate pathways involved in oncogenesis. In conclusion, this study contributes to the knowledge about the possible effects of chronic OA consumption.
Insights
Okadaic Acid (OA) at sublethal doses increases gastric and colon cell proliferation by activating oncogenic pathways like Erk and Akt. This study highlights potential risks of chronic OA exposure.
Area of Science:
- Toxicology
- Cell Biology
- Oncology
Background:
- Okadaic Acid (OA) is a toxin targeting gastric and colon epithelial cells.
- Sublethal OA doses may activate signaling pathways involved in cell growth and cancer.
- Protein phosphatase 2A (PP2A) is a key target for OA's cellular effects.
Purpose of the Study:
- To investigate the effect of Okadaic Acid (OA) on gastric and colon epithelial cell proliferation.
- To determine if OA activates Erk and Akt signaling pathways at sublethal concentrations.
- To elucidate the role of OA in cellular oncogenesis.
Main Methods:
- Dose-response and time-course experiments using OA on AGS, MKN-45, and Caco 2 cell lines.
- Analysis of cell proliferation rates at various OA exposure times (4h, 24h, 48h).
- Assessment of Cyclin B overexpression and activation of Akt and Erk signaling pathways.
Main Results:
- Sublethal OA doses significantly increased cell proliferation in gastric and colon cell lines after 24h or 48h exposure.
- OA exposure led to overexpression of Cyclin B, promoting cell cycle progression (G2 to mitosis).
- OA induced activation of Akt and Erk signaling pathways in all tested cell lines.
Conclusions:
- Okadaic Acid promotes proliferation of gastric and colon epithelial cells at sublethal doses.
- OA activates key signaling pathways (Akt, Erk) implicated in oncogenesis.
- Findings suggest potential risks associated with chronic Okadaic Acid consumption.
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