Berbamine Inhibits the Biological Activities of Prostate Cancer Cells by Modulating the ROS/NF-κB Axis


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Background/Introduction:Prostate cancer ranks as the second leading cause of cancer death. No effective pharmacological agent is available for prostate cancer treatment. Berbamine is an alkaloid extracted from the Chinese herb berberis, which exerts an effect on inhibiting cancer cell proliferation.

Objective: This study aimed to explore the mechanism of berbamine in inhibiting prostate cancer.

Methods: Prostate cancer cell lines PC-3 and DU145 cells were used to evaluate the effects of berbamine. Cell viability was determined using cell-counting kit 8. The intracellular reactive oxygen species (ROS) levels were measured using a ROS assay kit. Cell apoptosis rate was examined using flow cytometry. The protein levels associated with cell proliferation, NF-κB pathway, and apoptosis were determined using western blot.

Results: It was found that berbamine induced cell cycle arrest in the S phase and inhibited prostate cancer cell growth and proliferation. Berbamine inhibited prostate cancer cells by inhibiting the activation of the NF-κB pathway in vitro. Berbamine increased ROS as an upstream molecule that inhibited the NF-κB pathway.

Conclusion: Our results demonstrated that berbamine can effectively reduce the proliferation of prostate cancer cells. The ROS/NF-κB axis plays a crucial role in berbamine-mediated anti-prostate cancer cell proliferation.

Sobre autores

Wanli Zhao

Department of Urology,, the Third Hospital of Hebei Medical University

Email: info@benthamscience.net

Yuqing Jiang

Department of Urology, Third Hospital of Hebei Medical University

Email: info@benthamscience.net

Xiaopeng Jia

Department of Urology,, the Third Hospital of Hebei Medical University

Email: info@benthamscience.net

Xiuli Wang

Department of Anesthesiology, The Third Hospital of Hebei Medical University

Email: info@benthamscience.net

Yuexian Guo

Department of Urology,, the Third Hospital of Hebei Medical University,

Autor responsável pela correspondência
Email: info@benthamscience.net

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