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<p>Cellular metabolism has emerged as a pivotal factor influencing the viability and functionality of cancer cells. To satisfy their substantial anabolic requirements, tumor cells adopt a distinct metabolic reprogramming divergent from that of non-transformed somatic cells. This review aims to examine metabolic reprogramming in head and neck squamous cell carcinoma (HNSCC), examining its role as a fundamental aspect of cancer progression and resistance to treatment. The article systematically summarizes the key mechanisms of metabolic reprogramming in HNSCC, including enhanced glycolysis, remodeling of amino acid metabolism, and dysregulation of lipid synthesis, and discusses how these metabolic pathways facilitate tumor proliferation and metastasis by influencing the microenvironment, antioxidant defenses, and resistance to ferroptosis. Additionally, the review examines the dynamic interactions between metabolic reprogramming and the tumor microenvironment, particularly focusing on HIF-1α-driven metabolic adaptation and immune evasion mechanisms under hypoxic conditions. Finally, the potential of metabolic-targeted therapies is discussed, highlighting future research directions and their applications in personalized treatment strategies.</p>

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Cancer metabolism: bridging tumorigenesis mechanisms to treatment susceptibility

  • 期刊论文

  • 发表日期：

    2025年9月28日

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  • Ji’an Liu,
  • Dan Shan,
  • Zhaokai Zhou,
  • Xutao Wen,
  • Rao Fu,
  • Bo Xu,
  • Peng Luo,
  • Zhengrui Li,
  • Ling Zhang

摘要

Cellular metabolism has emerged as a pivotal factor influencing the viability and functionality of cancer cells. To satisfy their substantial anabolic requirements, tumor cells adopt a distinct metabolic reprogramming divergent from that of non-transformed somatic cells. This review aims to examine metabolic reprogramming in head and neck squamous cell carcinoma (HNSCC), examining its role as a fundamental aspect of cancer progression and resistance to treatment. The article systematically summarizes the key mechanisms of metabolic reprogramming in HNSCC, including enhanced glycolysis, remodeling of amino acid metabolism, and dysregulation of lipid synthesis, and discusses how these metabolic pathways facilitate tumor proliferation and metastasis by influencing the microenvironment, antioxidant defenses, and resistance to ferroptosis. Additionally, the review examines the dynamic interactions between metabolic reprogramming and the tumor microenvironment, particularly focusing on HIF-1α-driven metabolic adaptation and immune evasion mechanisms under hypoxic conditions. Finally, the potential of metabolic-targeted therapies is discussed, highlighting future research directions and their applications in personalized treatment strategies.