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Radiosensitivity of Cancer Stem Cells in Lung Cancer Cell Lines
Published on: August 21, 2019
Biochanin A Induces S Phase Arrest and Apoptosis in Lung Cancer Cells
Yan Li1, Haiyang Yu1, Fengfeng Han1
1Department of Respiratory Medicine, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, China.
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.
Insights
Biochanin A shows promise as a lung cancer treatment by inhibiting cancer cell proliferation and inducing apoptosis. This study reveals its mechanisms, suggesting potential for new lung cancer therapies.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Lung cancer has a low 5-year survival rate, necessitating novel treatments.
- Effective therapeutic strategies for lung cancer are urgently required.
Purpose of the Study:
- To investigate the anticancer effects of Biochanin A on lung cancer.
- To elucidate the underlying mechanisms of Biochanin A's action in lung cancer cells.
Main Methods:
- Assessed cell viability, colony formation, cell cycle, and apoptosis in A549 and 95D lung cancer cells.
- Utilized subcutaneous xenograft models to evaluate in vivo efficacy.
- Analyzed the expression of cell cycle and apoptosis-related proteins (P21, Caspase-3, Bcl-2).
Main Results:
- Biochanin A significantly reduced lung cancer cell viability and colony formation.
- Induced S phase arrest, apoptosis, and decreased mitochondrial membrane potential.
- Inhibited tumor growth in vivo and modulated key protein expressions.
Conclusions:
- Biochanin A inhibits lung cancer proliferation by inducing cell cycle arrest and apoptosis.
- Mechanisms involve regulating cell cycle proteins and activating Bcl-2 and Caspase-3 pathways.
- Biochanin A presents a potential therapeutic candidate for lung cancer treatment.
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