{"title":"生物香豆素 A 通过线粒体途径和 Pi3K/AKT 抑制诱导 MCF-7 乳腺癌细胞凋亡","authors":"Dianxiu Wang, Chuyi Zheng, Bo Chen, Shuang Ma","doi":"10.1002/cbf.70014","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>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.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"42 8","pages":""},"PeriodicalIF":2.8000,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Biochanin A Induces Apoptosis in MCF-7 Breast Cancer Cells through Mitochondrial Pathway and Pi3K/AKT Inhibition\",\"authors\":\"Dianxiu Wang, Chuyi Zheng, Bo Chen, Shuang Ma\",\"doi\":\"10.1002/cbf.70014\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n <p>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.</p></div>\",\"PeriodicalId\":9669,\"journal\":{\"name\":\"Cell Biochemistry and Function\",\"volume\":\"42 8\",\"pages\":\"\"},\"PeriodicalIF\":2.8000,\"publicationDate\":\"2024-11-11\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cell Biochemistry and Function\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1002/cbf.70014\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Biochemistry and Function","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/cbf.70014","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
本研究旨在探讨生物黄酮素 A 抑制乳腺癌细胞增殖并诱导其凋亡的分子机制。将培养的 MCF-7 细胞分为四组:第 1 组为对照组,第 2、3 和 4 组分别用不同浓度的 Biochanin A 处理。处理后,对细胞进行监测,并在培养 24 小时后检测细胞的形态变化。结果表明,Biochanin A 可抑制细胞增殖、增加活性氧的形成并诱导细胞凋亡。此外,PCR 阵列分析表明,细胞周期蛋白 D3、细胞周期蛋白 B1、CDK1、CDK2 和 CDK4 的基因表达水平下调,而 p21、p27 和 p53 的表达水平显著上调。这些结果表明,Biochanin A 能抑制乳腺癌细胞的活力,并通过线粒体途径诱导细胞凋亡,同时还能抑制 Pi3K/Akt 信号通路和调节细胞周期标志物。
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.
期刊介绍:
Cell Biochemistry and Function publishes original research articles and reviews on the mechanisms whereby molecular and biochemical processes control cellular activity with a particular emphasis on the integration of molecular and cell biology, biochemistry and physiology in the regulation of tissue function in health and disease.
The primary remit of the journal is on mammalian biology both in vivo and in vitro but studies of cells in situ are especially encouraged. Observational and pathological studies will be considered providing they include a rational discussion of the possible molecular and biochemical mechanisms behind them and the immediate impact of these observations to our understanding of mammalian biology.