Zhang Juan, Su Hongzheng, Li Qingfeng, Li Jing, Zhao Qianfeng
Department of Oncology, Xiangyang Central Hospital, The Affiliated Hospital of Hubei College of Arts and Science, Xiangyang, Hubei 441021, P.R. China.
Department of Infectious Disease, Zaoyang First People's Hospital, Zaoyang, Hubei 441200, P.R. China.
Mol Med Rep. 2017 Apr;15(4):2296-2302. doi: 10.3892/mmr.2017.6260. Epub 2017 Feb 28.
Genistein is an important chemopreventive agent against atherosclerosis and cancer. However, whether genistein is effective in the treatment of lung cancer, and its underlying mechanism, remains to be determined. The present study demonstrated that genistein treatment of A549 lung cancer cells decreased viability in a dose‑ and time‑dependent manner, and induced apoptosis. Additionally, A549 cells exhibited significantly increased reactive oxygen species formation and cytochrome‑c leakage, and activated caspase‑3, B‑cell lymphoma 2‑associated X protein and apoptosis inducing factor expression levels, which are involved in the mitochondrial apoptosis pathway. Furthermore, the phosphatidylinositol‑4,5‑biphosphate 3‑kinase (PI3K)/protein kinase B (AKT)/hypoxia‑inducible factor‑1α (HIF‑1α) and nuclear factor‑κB (NF‑κB)/cyclooxygenase‑2 (COX‑2) signaling pathways were significantly downregulated by genistein treatment. In conclusion, reduced proliferation and increased apoptosis in A549 lung cancer cells was associated with inhibition of the PI3K/AKT/HIF‑1α/ and NF‑κB/COX‑2 signaling pathways, which implicates genistein as a potential chemotherapeutic agent for the treatment of lung cancer.
染料木黄酮是一种抗动脉粥样硬化和癌症的重要化学预防剂。然而，染料木黄酮在肺癌治疗中是否有效及其潜在机制仍有待确定。本研究表明，用染料木黄酮处理A549肺癌细胞会以剂量和时间依赖性方式降低细胞活力，并诱导细胞凋亡。此外，A549细胞表现出活性氧生成和细胞色素c泄漏显著增加，并激活了参与线粒体凋亡途径的半胱天冬酶-3、B细胞淋巴瘤2相关X蛋白和凋亡诱导因子的表达水平。此外，染料木黄酮处理显著下调了磷脂酰肌醇-4,5-二磷酸3激酶（PI3K）/蛋白激酶B（AKT）/缺氧诱导因子-1α（HIF-1α）和核因子-κB（NF-κB）/环氧化酶-2（COX-2）信号通路。总之，A549肺癌细胞增殖减少和凋亡增加与PI3K/AKT/HIF-1α和NF-κB/COX-2信号通路的抑制有关，这表明染料木黄酮是一种治疗肺癌的潜在化疗药物。
