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Inhibition of FSP1: A new strategy for the treatment of tumors (Review)
Qiangfang Dai1, Xiaoli Wei1, Jumei Zhao1
1School of Medicine, Yan'an University, Yan'an, Shaanxi 716000, P.R. China.
Abstract:
Ferroptosis, a regulated form of cell death, is intricately linked to iron‑dependent lipid peroxidation. Recent evidence strongly supports the induction of ferroptosis as a promising strategy for treating cancers resistant to conventional therapies. A key player in ferroptosis regulation is ferroptosis suppressor protein 1 (FSP1), which promotes cancer cell resistance by promoting the production of the antioxidant form of coenzyme Q10. Of note, FSP1 confers resistance to ferroptosis independently of the glutathione (GSH) and glutathione peroxidase‑4 pathway. Therefore, targeting FSP1 to weaken its inhibition of ferroptosis may be a viable strategy for treating refractory cancer. This review aims to clarify the molecular mechanisms underlying ferroptosis, the specific pathway by which FSP1 suppresses ferroptosis and the effect of FSP1 inhibitors on cancer cells.
Insights
Ferroptosis, a cell death process involving iron, offers new cancer treatment avenues. Inhibiting ferroptosis suppressor protein 1 (FSP1) may overcome treatment resistance by blocking its antioxidant CoQ10 production.
Area of Science:
- Biochemistry
- Cell Biology
- Oncology
Background:
- Ferroptosis is an iron-dependent form of regulated cell death.
- Inducing ferroptosis is a promising strategy for treating therapy-resistant cancers.
- Ferroptosis suppressor protein 1 (FSP1) confers resistance to ferroptosis.
Purpose of the Study:
- To clarify the molecular mechanisms of ferroptosis.
- To elucidate the FSP1 pathway in ferroptosis suppression.
- To review the effects of FSP1 inhibitors on cancer cells.
Main Methods:
- Literature review of ferroptosis mechanisms.
- Analysis of FSP1's role in lipid peroxidation and CoQ10 production.
- Examination of studies on FSP1 inhibitors in cancer models.
Main Results:
- FSP1 promotes cancer cell ferroptosis resistance via coenzyme Q10 production.
- FSP1-mediated resistance is independent of the glutathione pathway.
- FSP1 inhibition sensitizes cancer cells to ferroptosis.
Conclusions:
- Targeting FSP1 is a potential strategy to treat ferroptosis-resistant cancers.
- Understanding FSP1's mechanism is crucial for developing novel cancer therapies.
- FSP1 inhibitors show promise in overcoming therapeutic resistance.
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