AI Article Synopsis
- Berberine, an isoquinoline alkaloid, shows potential anticancer effects by reducing the viability of cervical cancer Ca Ski cells in a dose- and time-dependent manner.
- The compound promotes apoptosis in these cells by increasing the ratio of certain proteins (p53, Bax/Bcl-2), raising reactive oxygen species (ROS) levels, disrupting mitochondrial function, and activating caspase-3.
- Blocking the apoptotic pathway with a pan-caspase inhibitor or catalase inhibits berberine's effects, suggesting that ROS and ER stress play major roles in this cancer treatment mechanism.
Article Abstract
Berberine, an isoquinoline alkaloid, has been shown to possess anticancer properties in some cancer cell lines. Here, we report that in vitro treatment of cervical cancer Ca Ski cells with berberine decreased the percentage of viable Ca Ski cells in a dose-dependent and time-dependent manner. Berberine enhanced the apoptosis of Ca Ski cells with the induction of a higher ratio of p53 and Bax/Bcl-2 proteins, increased levels of reactive oxygen species (ROS) and Ca2+, disruption of the mitochondrial membrane potential, and promotion of caspase-3 activity. In CaSki cells pretreated with the pan-caspase inhibitor zVAD-fmk, the berberine-induced caspase-3 activity and apoptosis were significantly blocked as confirmed by flow cytometric analysis. Western blot also showed that berberine induced the expression of GADD153, a transcription factor involved in apoptosis. Thus berberine increased ROS levels leading to endoplasmic reticulum (ER) stress based on the increase of GADD153 and shown by Ca2+ release from the ER. When the Ca Ski cells were pretreated with catalase, GADD153 production was abrogated and apoptosis was significantly reduced.
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