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Published on: July 21, 2018
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Rapamycin inhibited the function of lung CSCs via SOX2
Li-Xia Xie1, Feng-Feng Sun1, Bin-Feng He2
1Department of Respiratory Diseases, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Summary
Rapamycin targets cancer stem cells (CSCs) in lung cancer by inhibiting SOX2 expression. This enhances cisplatin sensitivity and reduces tumor growth, offering a potential new therapeutic strategy.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Cancer stem cells (CSCs) drive lung cancer initiation, progression, and recurrence.
- Targeting CSCs is a promising strategy for effective lung cancer treatment.
Purpose of the Study:
- To investigate the effect of rapamycin on lung CSCs.
- To elucidate the role of SOX2 in rapamycin's anti-CSC activity.
Main Methods:
- Used A549 lung cancer cells.
- Administered rapamycin and cisplatin (DDP).
- Performed gene knockdown and ectopic expression of SOX2.
Main Results:
- Rapamycin inhibited mammalian target of rapamycin (mTOR) signaling and CSC properties (sphere formation, EMT).
- Rapamycin reduced SOX2 expression, enhancing cisplatin sensitivity.
- SOX2 knockdown mimicked rapamycin's effects; SOX2 overexpression conferred rapamycin resistance.
Conclusions:
- Rapamycin inhibits lung CSCs by downregulating SOX2.
- Targeting the SOX2 pathway with rapamycin is a potential therapeutic strategy for lung cancer.
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