Glucose metabolic reprogramming and its therapeutic potential in obesity-associated endometrial cancer

Endometrial cancer (EC) is a common gynecological cancer that endangers women health. Although substantial progresses of EC management have been achieved in recent years, the incidence of EC still remains high. Obesity has been a common phenomenon worldwide that increases the risk of EC. However, the mechanism associating obesity and EC has not been fully understood. Metabolic reprogramming as a remarkable characteristic of EC is currently emerging. As the primary factor of metabolic syndrome, obesity promotes insulin resistance, hyperinsulinemia and hyperglycaemia. This metabolic disorder remodels systemic status, which increases EC risk and is related with poor prognosis. Glucose metabolism in EC cells is complex and mediated by glycolysis and mitochondria to ensure energy requirement. Factors that affect glucose metabolism may have an impact on EC initiation and progression. In this study, we review the glucose metabolic reprogramming of EC not only systemic metabolism but also inherent tumor cell metabolism. In particular, the role of glucose metabolic regulation in malignant properties of EC will be focused. Understanding of metabolic profile and glucose metabolism-associated regulation mechanism in EC may provide novel perspective for treatment.

Automated summary

Endometrial cancer is a common gynecological cancer that poses a significant threat to women's health. Obesity, as a worldwide phenomenon, increases the risk of endometrial cancer, but the underlying mechanism is not fully understood. This study reviews the metabolic reprogramming of glucose in endometrial cancer, not only from a systemic perspective but also focusing on the tumor cell metabolism. Understanding the metabolic profile and the regulation mechanism associated with glucose metabolism in endometrial cancer may offer novel perspectives for treatment.