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Published on: August 23, 2019
Berberine triggers apoptosis through the PI3K/Akt pathways and Nrf2 by inducing ROS in papillary thyroid cancer
1Department of Endocrinology, The General Hospital of Central Theater Command, Wuhan, 430070, China; The First School of Clinical Medicine, Southern Medical University, Guangzhou, 510180, China.
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.
Insights
Berberine (BBR) effectively inhibits papillary thyroid cancer (PTC) growth by targeting the Nrf2 pathway. This natural compound promotes cancer cell death and may offer a new therapeutic strategy for PTC.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Nuclear factor erythroid 2-related factor 2 (Nrf2) is overexpressed in papillary thyroid cancer (PTC), correlating with poor patient outcomes.
- Berberine (BBR) demonstrates potential anticancer properties by reducing Nrf2 levels and inducing apoptosis in cancer cells.
- The precise molecular mechanisms of BBR's anticancer effects in PTC require further elucidation.
Purpose of the Study:
- To investigate the anticancer effects of Berberine (BBR) on papillary thyroid cancer (PTC) cells.
- To elucidate the molecular mechanisms underlying BBR's efficacy in PTC.
- To evaluate the therapeutic potential of BBR for PTC treatment.
Main Methods:
- Cell apoptosis was assessed using MTT assays and flow cytometry.
- In vivo antitumor efficacy was evaluated using a xenograft mouse model.
- Molecular and biochemical techniques were employed to determine BBR's mechanism of action.
Main Results:
- BBR significantly inhibited PTC cell proliferation and induced apoptosis.
- Administration of BBR via gavage reduced xenograft tumor development in vivo.
- BBR was found to inhibit the Nrf2-dependent PI3K/Akt signaling pathway, leading to increased reactive oxygen species (ROS) production.
Conclusions:
- BBR targets PTC by inhibiting the Nrf2 and PI3K/Akt signaling pathways via ROS generation.
- These findings suggest that BBR holds promise as a potential therapeutic agent for papillary thyroid cancer.
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