For example, glucose restriction in hepatocellular carcinoma cells could down‐regulate HSF‐1 expression, resulting in direct suppression of Snail 1 expression and up‐regulating of E‐cadherin expression, thus inhibiting EMT‐associated migration and invasion.39 In uterus endometrial cancer cells, high glucose could promote EMT and lead to a high level of viability and invasion through increasing Glut4 and VEGF/VEGFR expression.34 However, the effect and mechanism of tumour glycolysis on EMT and metastasis of OSCC is still largely unknown. The gene discussed is KDR; the disease is hepatocellular carcinoma.