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大豆素 A 诱导肺癌细胞 S 期阻滞和凋亡。

Biochanin A Induces S Phase Arrest and Apoptosis in Lung Cancer Cells.

机构信息

Department of Respiratory Medicine, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, China.

出版信息

Biomed Res Int. 2018 Oct 3;2018:3545376. doi: 10.1155/2018/3545376. eCollection 2018.

DOI:10.1155/2018/3545376
PMID:30402472
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6192129/
Abstract

Lung cancer is among the most common malignancies with a poor 5-year survival rate reaching only 16%. Thus, new effective treatment modalities and drugs are urgently needed for the treatment of this malignancy. In this study, we conducted the first investigation of the effects of Biochanin A on lung cancer and revealed the mechanisms underlying its potential anticancer effects. Biochanin A decreased cell viability in a time-dependent and dose-dependent manner and suppressed colony formation in A549 and 95D cells. In addition, Biochanin A induced S phase arrest and apoptosis and decreased mitochondrial membrane potential (ΔΨm) in A549 and 95D cells in a dose-dependent manner. Our results of subcutaneous xenograft models showed that the growth of Biochanin A group was significantly inhibited compared with that of control groups. Finally, P21, Caspase-3, and Bcl-2 were activated in Biochanin A-treated cells and Biochanin A-treated xenografts which also demonstrated that Biochanin A induced cell cycle arrest and apoptosis in lung cancer cells by regulating expression of cell cycle-related proteins and apoptosis-related proteins. In conclusion, this study suggests that Biochanin A inhibits the proliferation of lung cancer cells and induces cell cycle arrest and apoptosis mainly by regulating cell cycle-related protein expression and activating the Bcl-2 and Caspase-3 pathways, thus suggesting that Biochanin A may be a promising drug to treat lung cancer.

摘要

肺癌是最常见的恶性肿瘤之一，5 年生存率仅为 16%。因此，迫切需要新的有效治疗方法和药物来治疗这种恶性肿瘤。在这项研究中，我们首次研究了大豆素 A 对肺癌的影响，并揭示了其潜在抗癌作用的机制。大豆素 A 呈时间和剂量依赖性地降低细胞活力并抑制 A549 和 95D 细胞的集落形成。此外，大豆素 A 以剂量依赖性方式诱导 A549 和 95D 细胞的 S 期阻滞和凋亡，并降低线粒体膜电位（ΔΨm）。我们的皮下异种移植模型结果表明，与对照组相比，大豆素 A 组的生长明显受到抑制。最后，大豆素 A 处理的细胞和大豆素 A 处理的异种移植物中激活了 P21、Caspase-3 和 Bcl-2，这也表明大豆素 A 通过调节细胞周期相关蛋白和凋亡相关蛋白的表达诱导肺癌细胞的细胞周期阻滞和凋亡。总之，本研究表明大豆素 A 通过调节细胞周期相关蛋白的表达和激活 Bcl-2 和 Caspase-3 途径抑制肺癌细胞的增殖并诱导细胞周期阻滞和凋亡，这表明大豆素 A 可能是治疗肺癌的一种有前途的药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ad1/6192129/93497bf12708/BMRI2018-3545376.014.jpg
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