Long-term exposure to low levels of okadaic acid accelerates cell cycle progression in colonic epithelial cells via p53 and Jak/Stat3 signaling pathways

As a major component of diarrheic shellfish poisoning (DSP) toxins, okadaic acid (OA) is widely distributed worldwide, and causes a series of serious public health problems. In colon tissue, previous studies have shown that high doses of OA can affect various intracellular processes, including destroy intercellular communication at gap junctions, induce cell apoptosis and trigger cell cycle arrest. However, there is a scarcity of studies on the effect and mechanism of action of low doses of OA in colonic tissues. In this study, we observed that exposure to low levels of OA altered cell cycle progression in vitro and in vivo. Investigation of the underlying mechanism revealed that OA induced alterations in the cell cycle by inhibiting the p53 signaling pathway or inducing the Jak/ Stat3 signaling pathway. In conclusion, this study provides novel insights into the effect and mechanism un-derlying long-term exposure to low levels of OA.