Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Sep 2:12:993775.
doi: 10.3389/fonc.2022.993775. eCollection 2022.

Berberine as a potential agent for breast cancer therapy

Affiliations
Review

Berberine as a potential agent for breast cancer therapy

Xiao-Dan Zhong et al. Front Oncol. .

Abstract

Breast cancer (BC) is a common malignancy that mainly occurred in women and it has become the most diagnosed cancer annually since 2020. Berberine (BBR), an alkaloid extracted from the Berberidacea family, has been found with broad pharmacological bioactivities including anti-inflammatory, anti-diabetic, anti-hypertensive, anti-obesity, antidepressant, and anticancer effects. Mounting evidence shows that BBR is a safe and effective agent with good anticancer activity against BC. However, its detailed underlying mechanism in BC treatment remains unclear. Here, we will provide the evidence for BBR in BC therapy and summarize its potential mechanisms. This review briefly introduces the source, metabolism, and biological function of BBR and emphasizes the therapeutic effects of BBR against BC via directly interacting with effector proteins, transcriptional regulatory elements, miRNA, and several BBR-mediated signaling pathways. Moreover, the novel BBR-based therapeutic strategies against BC improve biocompatibility and water solubility, and the efficacies of BBR are also briefly discussed. Finally, the status of BBR in BC treatment and future research directions is also prospected.

Keywords: Breast cancer; apoptosis; autophagic; berberine; cell cycle arrest.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Schematic illustration of the effect of BBR on signaling pathways of apoptosis and cell cycle arrest in BC.

References

    1. Siegel RL, Miller KD, Fuchs HE, Jemal A. Cancer statistics, (2022). CA Cancer J Clin (2022) 72:7–33. doi: 10.3322/caac.21708 - DOI - PubMed
    1. Cheng SS, Yang GJ, Wang WH, Song YQ, Ko CN, Han QB, et al. Identification of a cytisine-based EED-EZH2 protein-protein interaction inhibitor preventing metastasis in triple-negative breast cancer cells. Acta Materia Med (2022) 1:197–211. doi: 10.15212/AMM-2022-0006 - DOI
    1. Yang GJ, Ko CN, Zhong HJ, Leung CH, Ma DL. Structure-based discovery of a selective KDM5A inhibitor that exhibits anti-cancer activity via inducing cell cycle arrest and senescence in breast cancer cell lines. Cancers (2019) 11(1):92. doi: 10.3390/cancers11010092 - DOI - PMC - PubMed
    1. Cheng SS, Qu YQ, Wu J, Yang GJ, Liu H, Wang W, et al. Inhibition of the CDK9–cyclin T1 protein–protein interaction as a new approach against triple-negative breast cancer. Acta Pharm Sin B (2022) 12:1390–405. doi: 10.1016/j.apsb.2021.10.024 - DOI - PMC - PubMed
    1. Cheng SS, Yang GJ, Wang WH, Ma DL, Leung CH. Discovery of a tetrahydroisoquinoline-based CDK9-cyclin T1 protein–protein interaction inhibitor as an anti-proliferative and anti-migration agent against triple-negative breast cancer cells. Genes Dis (2021). doi: 10.1016/j.gendis.2021.06.005 - DOI - PMC - PubMed

LinkOut - more resources