Biochanin A Induces Apoptosis in MCF‐7 Breast Cancer Cells through Mitochondrial Pathway and Pi3K/AKT Inhibition

The study aimed to investigate the molecular mechanisms by which Biochanin A inhibits proliferation and induces apoptosis in breast cancer cells. Cultured MCF-7 cells were divided into four groups: Group 1-control, while Groups 2, 3, and 4 were treated with Biochanin A at different concentrations. After treatment, the cells were monitored, and morphological changes were examined after 24 h of incubation. The results showed that Biochanin A inhibited cell proliferation, increased reactive oxygen species formation, and induced apoptosis. Furthermore, western blot analysis revealed that Biochanin A-treated cells exhibited lower expression of the Bcl-2, p-PI3K and p-AKT and higher expression of proapoptotic genes, including Bax, Caspase-3, Caspase-9, and cytochrome c. Additionally, PCR array analysis indicated that the gene expression levels of cyclin D3, cyclin B1, CDK1, CDK2, and CDK4 were downregulated, while the expression levels of p21, p27, and p53 were significantly upregulated. These results suggest that Biochanin A can suppress the viability of breast cancer cells and induce apoptosis via the mitochondrial pathway, along with inhibition of the Pi3K/Akt signaling pathway and modulation of cell cycle markers.

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Publication Details

Journal
Cell Biochemistry and Function
Published
2024-11-11
DOI
https://doi.org/10.1002/cbf.70014
Citations
6
Primary Topic
Cancer-related Molecular Pathways
Type
article
Field-Weighted Citation Impact
1.70
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article

Biochanin A Induces Apoptosis in MCF‐7 Breast Cancer Cells through Mitochondrial Pathway and Pi3K/AKT Inhibition

Chuyi Zheng, Bo Chen, Shuang Ma, Dianxiu Wang
6 citations
Cell Biochemistry and Function
Cancer-related Molecular Pathways
1.70
article

Biochanin A Induces Apoptosis in MCF‐7 Breast Cancer Cells through Mitochondrial Pathway and Pi3K/AKT Inhibition

Chuyi Zheng, Bo Chen, Shuang Ma, Dianxiu Wang
article en
6 citations

Abstract

The study aimed to investigate the molecular mechanisms by which Biochanin A inhibits proliferation and induces apoptosis in breast cancer cells. Cultured MCF-7 cells were divided into four groups: Group 1-control, while Groups 2, 3, and 4 were treated with Biochanin A at different concentrations. After treatment, the cells were monitored, and morphological changes were examined after 24 h of incubation. The results showed that Biochanin A inhibited cell proliferation, increased reactive oxygen species formation, and induced apoptosis. Furthermore, western blot analysis revealed that Biochanin A-treated cells exhibited lower expression of the Bcl-2, p-PI3K and p-AKT and higher expression of proapoptotic genes, including Bax, Caspase-3, Caspase-9, and cytochrome c. Additionally, PCR array analysis indicated that the gene expression levels of cyclin D3, cyclin B1, CDK1, CDK2, and CDK4 were downregulated, while the expression levels of p21, p27, and p53 were significantly upregulated. These results suggest that Biochanin A can suppress the viability of breast cancer cells and induce apoptosis via the mitochondrial pathway, along with inhibition of the Pi3K/Akt signaling pathway and modulation of cell cycle markers.

Cell Biochemistry and FunctionVol. 42(8)
Shanghai University (CN), Shanghai University of Traditional Chinese Medicine (CN), First Affiliated Hospital of Chengdu Medical College (CN), Songjiang District Central Hospital (CN), Anyang Hospital of Traditional Chinese Medicine (CN)
Good health and well-being
Openalex Percentile: Top 13%
Cancer-related Molecular Pathways
1.70
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Biochanin A Induces Apoptosis in MCF‐7 Breast Cancer Cells through Mitochondrial Pathway and Pi3K/AKT Inhibition — Chuyi Zheng, Bo Chen, et al. · Cell Biochemistry and Function (2024) | TGRS Research Map | TGRS