Abstract

Cancer metabolic reprogramming had been widely recognised as a critical mechanism underlying tumour proliferation and drug resistance, yet the quantitative relationship between metabolic alterations and therapeutic resistance required further clarification. This study had examined the role of glycolysis, mitochondrial respiration, and glutamine metabolism in cancer cell proliferation and drug resistance using quantitative experimental analysis. The findings had demonstrated that increased glycolytic activity enhanced proliferation rate by over 80 percent, while enhanced mitochondrial respiration increased drug resistance by approximately 49 percent. Glutamine metabolism had also been shown to significantly increase cancer cell survival, confirming its role in tumour viability. Correlation analysis had revealed strong positive relationships between metabolic activity and proliferation as well as drug resistance, with correlation coefficients ranging from 0.79 to 0.88. These findings had supported metabolic control theory and evolutionary adaptation theory, which explained metabolic flexibility and therapeutic resistance in cancer cells. The study had concluded that metabolic reprogramming represented a fundamental driver of tumour progression and drug resistance. Therefore, targeting metabolic pathways could improve therapeutic effectiveness and reduce treatment failure. These findings had important implications for cancer therapy development and provided a foundation for future metabolic targeting strategies.