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Article

Genistein decreases A549 cell viability via inhibition of the PI3K/AKT/HIF‑1α/VEGF and NF‑κB/COX‑2 signaling pathways

  • Authors:
    • Juan Zhang
    • Hongzheng Su
    • Qingfeng Li
    • Jing Li
    • Qianfeng Zhao
  • View Affiliations / Copyright

    Affiliations: 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
  • Pages: 2296-2302
    |
    Published online on: February 28, 2017
       https://doi.org/10.3892/mmr.2017.6260
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Abstract

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.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang J, Su H, Li Q, Li J and Zhao Q: Genistein decreases A549 cell viability via inhibition of the PI3K/AKT/HIF‑1α/VEGF and NF‑κB/COX‑2 signaling pathways. Mol Med Rep 15: 2296-2302, 2017.
APA
Zhang, J., Su, H., Li, Q., Li, J., & Zhao, Q. (2017). Genistein decreases A549 cell viability via inhibition of the PI3K/AKT/HIF‑1α/VEGF and NF‑κB/COX‑2 signaling pathways. Molecular Medicine Reports, 15, 2296-2302. https://doi.org/10.3892/mmr.2017.6260
MLA
Zhang, J., Su, H., Li, Q., Li, J., Zhao, Q."Genistein decreases A549 cell viability via inhibition of the PI3K/AKT/HIF‑1α/VEGF and NF‑κB/COX‑2 signaling pathways". Molecular Medicine Reports 15.4 (2017): 2296-2302.
Chicago
Zhang, J., Su, H., Li, Q., Li, J., Zhao, Q."Genistein decreases A549 cell viability via inhibition of the PI3K/AKT/HIF‑1α/VEGF and NF‑κB/COX‑2 signaling pathways". Molecular Medicine Reports 15, no. 4 (2017): 2296-2302. https://doi.org/10.3892/mmr.2017.6260
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang J, Su H, Li Q, Li J and Zhao Q: Genistein decreases A549 cell viability via inhibition of the PI3K/AKT/HIF‑1α/VEGF and NF‑κB/COX‑2 signaling pathways. Mol Med Rep 15: 2296-2302, 2017.
APA
Zhang, J., Su, H., Li, Q., Li, J., & Zhao, Q. (2017). Genistein decreases A549 cell viability via inhibition of the PI3K/AKT/HIF‑1α/VEGF and NF‑κB/COX‑2 signaling pathways. Molecular Medicine Reports, 15, 2296-2302. https://doi.org/10.3892/mmr.2017.6260
MLA
Zhang, J., Su, H., Li, Q., Li, J., Zhao, Q."Genistein decreases A549 cell viability via inhibition of the PI3K/AKT/HIF‑1α/VEGF and NF‑κB/COX‑2 signaling pathways". Molecular Medicine Reports 15.4 (2017): 2296-2302.
Chicago
Zhang, J., Su, H., Li, Q., Li, J., Zhao, Q."Genistein decreases A549 cell viability via inhibition of the PI3K/AKT/HIF‑1α/VEGF and NF‑κB/COX‑2 signaling pathways". Molecular Medicine Reports 15, no. 4 (2017): 2296-2302. https://doi.org/10.3892/mmr.2017.6260
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