Berberine triggers apoptosis through the PI3K/Akt pathways and Nrf2 by inducing ROS in papillary thyroid cancer.

BACKGROUND

Nrf2 is highly expressed in papillary thyroid cancer (PTC) and is associated with negative outcomes. Research has indicated that Berberine (BBR) can lower Nrf2 levels and trigger apoptosis in cancer cells. However, the exact molecular mechanisms behind its anticancer effects in PTC are not fully understood.

METHODS

The effects of BBR on cell apoptosis were assessed using the MTT assay and flow cytometry. To evaluate BBR's in vivo antitumor efficacy, a xenograft model was used. Molecular and biochemical methods were applied to clarify the mechanisms through which BBR exerts its anticancer effects in PTC.

RESULTS

BBR has been shown to effectively inhibit the growth of PTC cells and promote programmed cell death. A higher dose of BBR administered via gavage significantly reduced the development of xenograft tumors. Mechanistically, BBR inhibits the Nrf2-dependent pathway of PI3K/Akt signaling pathway, resulting in the production of reactive oxygen species (ROS).

CONCLUSIONS

Our results suggest indicate that BBR can target PTC by inhibiting the Nrf2 and PI3K/Akt pathways through ROS generation. This indicats that BBR may serve as a potential therapeutic agent for PTC treatment.