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Curcumin Induces Ferroptosis in A549 CD133+ Cells through the GSH-GPX4 and FSP1-CoQ10-NAPH Pathways.
Jiajing Zhou1, Lanyue Zhang2, Jifeng Yan3
1Department of Oncology, Yantai Hospital of Traditional Chinese Medicine, 264001 Yantai, Shandong, China.
Discovery Medicine
|June 5, 2023
Summary
Curcumin induces ferroptosis in lung cancer stem cells by inhibiting key pathways, reducing their self-renewal and tumorigenic potential. This offers a promising therapeutic strategy for lung cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Lung cancer stem cells (LCSCs) possess unlimited proliferation and self-renewal capabilities, making them key targets for cancer therapy.
- Targeting LCSCs-related signaling pathways presents a promising therapeutic strategy for lung cancer.
- Ferroptosis, a form of regulated cell death, is an emerging strategy for LCSCs treatment, with curcumin identified as a potential inducer.
Purpose of the Study:
- To investigate the effects of curcumin on lung cancer stem cells (LCSCs) through ferroptosis-related pathways.
- To analyze the impact of curcumin on the tumorigenic and self-renewal abilities of LCSCs.
- To elucidate the specific molecular mechanisms by which curcumin induces ferroptosis in LCSCs.
Main Methods:
- Isolation of A549 CD133+ and A549 CD133- cells using magnetic bead-based separation.
- Assessment of tumorigenic ability via colony formation, sphere formation assays, and xenografting in NOD/SCID mice.
- Treatment of A549 CD133+ cells with varying curcumin doses and measurement of cell viability, GPX4, and FSP1 expression.
Main Results:
- A549 CD133+ cells exhibited significantly higher tumorigenic potential compared to A549 cells.
- Curcumin treatment suppressed the expression of glutathione peroxidase 4 (GPX4) and ferroptosis suppressor protein 1 (FSP1) in A549 CD133+ cells, inducing ferroptosis.
- The effects of curcumin were abrogated by the ferroptosis inhibitor ferrostatin-1 (Fer-1), confirming the ferroptosis-dependent mechanism.
Conclusions:
- Curcumin induces ferroptosis in LCSCs by inhibiting the glutathione-GPX4 and FSP1-CoQ10-NADH pathways.
- This ferroptosis induction by curcumin leads to the suppression of self-renewal potential in LCSCs.
- Curcumin represents a potential therapeutic agent for lung cancer by targeting LCSCs through ferroptosis induction.
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