Epidemiological studies have shown that abnormal glucose and lipid metabolism is associated with a variety of malignant tumors, including oral squamous cell carcinoma. In this paper, the role of abnormal glucose and lipid metabolism, especially diabetes mellitus and obesity, in the occurrence and development of oral squamous cell carcinoma and its pathogenesis are reviewed based on the research results of our group and the literature. Hyperglycemia and insulinemia in diabetes mellitus are the main mechanisms that increase the risk of cancer. Our research shows that hyperglycemia can promote the proliferation, invasion and metastasis of tongue squamous cell carcinoma through the glycolytic enzyme M2 pyruvate kinase (PKM2) and hexokinase 2 (HK2). Hyperinsulinemia can promote the proliferation, invasion and metastasis of tongue squamous cell carcinoma by activating the insulin-like growth factor signal transduction system. Obese patients are often accompanied by increased serum adipokine Chemerin (Chem). Our study shows that serum Chem concentrations in obese patients with tongue cancer are significantly higher compared with nonobese patients. Chem can regulate the proliferation, invasion and migration of tongue squamous cell carcinoma cells through the SOD2-H₂O₂ signaling pathway. These results provide a basis for the prevention of oral squamous cell carcinoma, provide a new iqdea for the precise treatment of oral squamous cell carcinoma, and suggest that the treatment of oral squamous cell carcinoma should also actively treat patients with diabetes and obesity.

Tongue squamous cell carcinoma (TSCC) is the most common cancer of head and neck malignancies. Despite advances in therapeutic management, the prognosis for TSCC patients has remained poor. Local or regional relapse and cervical lymph node metastasis are clinical challenges. This review has introduced the research progress on cancer invasion and metastasis related genes, micro RNAs, EMT and cancer stem cells behavior and so on. With the further study on the mechanisms of invasion and metastasis of TSCC, the difficulties might be overcome.