Advances in the study of regulators of ferroptosis in head and neck squamous cell carcinoma (Review)

Abstract

Head and neck squamous cell carcinoma (HNScc), a common malignancy of the head and neck, is associated with a rapid progression, a high mortality rate and unsatisfactory curative effects. The treatment efficacy is unsatisfactory due to chemotherapeutic drug resistance, the lack of ideal therapeutic agents, as well as the absence of clinical prognostic models. Thus, the identification of novel potential therapeutic targets for its diagnosis and treatment is vital. Ferroptosis is an iron-dependent regulatory cell death mode different from traditional cell death modes, such as apoptosis and autophagy, and has notable therapeutic potential in cancer treatment. The study of ferroptosis in HNScc is expected to solve this bottleneck problem. In the present review, the findings, characteristics and regulatory mechanisms of ferroptosis are summarized, with emphasis on the factors and drugs that regulate ferroptosis in HNScc, in order to provide theoretical basis for the targeted therapy of ferroptosis in HNScc. Contents1. Introduction 2. data collection methods 3. The discovery and characteristics of ferroptosis 4. Regulatory mechanisms of ferroptosis 5. Ferroptosis regulators in head and neck squamous cell carcinoma 6. Therapeutic modalities regulating ferroptosis in head and neck squamous carcinoma 7. conclusions and future perspectives

Cuproptosis-related gene subtypes predict prognosis in patients with head and neck squamous cell carcinoma

“…Many anticancer drugs (Dabrafenib, vemurafenib,Val-boroPro) show a profound effect on programmed cell death, implied that programmed cell death,such as apoptosis,autophagy,ferroptosis,may play a role in cancer therapy [ 30 ]. Previous studies have shown that we can reduce cisplatin resistance in cancer cells, and enhance the sensitivity of tumor cells to chemotherapeutic drugs by promoting ferroptosis in tumor cells [ 31 ]. With the development of anticancer therapies that selectively induce cancer cell death, cuproptosis may become a new target for the treatment of HNSCC.…”

Depletion of effector regulatory T cells drives major response to induction dual immune checkpoint blockade

“…6a, Supplementary Table 11). For example, expression of CCL5, a proinflammatory chemokine for NK and other immune cells, was higher in MHRs, whereas expression of Ferritin Heavy Chain 1 (FTH1), associated with Treg recruitment and poor OS in HNSCC 42 , was higher in nMHRs. Gene set enrichment analysis (GSEA) revealed that several hallmark immune response pathways (e.g., interferon alpha and gamma response) were enriched in MHRs relative to nMHRs at baseline (Extended Data Fig.…”