Effect of regulatory cell death on the occurrence and development of head and neck squamous cell carcinoma

Abstract

Head and neck cancer is a malignant tumour with a high mortality rate characterized by late diagnosis, high recurrence and metastasis rates, and poor prognosis. Head and neck squamous cell carcinoma (HNSCC) is the most common type of head and neck cancer. Various factors are involved in the occurrence and development of HNSCC, including external inflammatory stimuli and oncogenic viral infections. In recent years, studies on the regulation of cell death have provided new insights into the biology and therapeutic response of HNSCC, such as apoptosis, necroptosis, pyroptosis, autophagy, ferroptosis, and recently the newly discovered cuproptosis. We explored how various cell deaths act as a unique defence mechanism against cancer emergence and how they can be exploited to inhibit tumorigenesis and progression, thus introducing regulatory cell death (RCD) as a novel strategy for tumour therapy. In contrast to accidental cell death, RCD is controlled by specific signal transduction pathways, including TP53 signalling, KRAS signalling, NOTCH signalling, hypoxia signalling, and metabolic reprogramming. In this review, we describe the molecular mechanisms of nonapoptotic RCD and its relationship to HNSCC and discuss the crosstalk between relevant signalling pathways in HNSCC cells. We also highlight novel approaches to tumour elimination through RCD.

Ferroptosis and EMT: key targets for combating cancer progression and therapy resistance

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Ferroptosis: a new regulatory mechanism in neuropathic pain

“…Two enzymes play a key role in the synthesis of PUFAs during the onset of iron death: acyl-coenzyme A synthase long-chain family member 4 (ACSL4) and lysophosphatidylcholine acyltransferase 3 (LPCAT3; Xue et al, 2023 ). When these two genes were knocked out, PUFA synthesis was reduced, causing the inhibition of ferroptosis.…”

Up-regulated ORC1 promotes lung adenocarcinoma by inhibiting ferroptosis via SLC7A11 dependent pathway

“…Dysregulation of ACSL4 has been implicated in promoting or inhibiting ferroptosis in different cellular contexts, making it an important player in the regulation of lipid metabolism and cell death pathways [ 19 ]. Furthermore, recent studies[ [ 19 , 20 ]] have highlighted the role of ACSL4 as a biomarker and potential therapeutic target in cancer, underscoring its significance in the context of (LUAD and the potential impact on the overall understanding of ferroptosis in cancer biology. Abnormal metabolic mechanisms associated with cancer ferroptosis offers the potential for developing latent effective therapeutic targets.…”