［］Tumor drug resistance is one of the primary causes of clinical therapy failure. According to conventional wisdom, resistance is mostly caused by accelerated DNA repair, decreased apoptosis, and greater drug efflux. More and more studies in recent years suggests that metabolic reprogramming, more especially the reprogramming of glucose metabolism, is a key factor in controlling tumor treatment resistance. This process is a crucial method by which tumor cells acquire advantages in survival and proliferation by adapting to the particular tumor microenvironment. The abnormally active aerobic glycolysis and pentose phosphate pathway in tumor cells can affect drug tolerance through pathways like regulating redox homeostasis, enhancing cellular stemness, and reshaping the tumor microenvironment, in addition to providing sustained material and energy supplies for rapid growth and proliferation. Additionally, combo treatments that target glycometabolic reprogramming in addition to anticancer medications have shown progressively greater therapeutic benefits. In an effort to offer fresh insights into the growing problem of tumor cell drug resistance, this review outlines the state of research on glucose metabolism reprogramming in different anticancer drug resistances.