Cancer cells undergo metabolic reprogramming to support rapid proliferation, often exhibiting enhanced glycolysis and mitochondrial dysfunction. This study investigates the interplay between glycolytic activity and mitochondrial impairment in cancer progression. It is hypothesized that targeting glycolysis in cancer cells with compromised mitochondrial function will impede tumor growth. Using breast cancer cell lines with induced mitochondrial dysfunction, glycolytic flux, cell proliferation, and apoptosis were assessed following treatment with a glycolysis inhibitor. Findings reveal that cells with mitochondrial dysfunction exhibit a significant increase in glycolytic activity compared to controls (p < 0.01). Inhibition of glycolysis in these cells resulted in a marked decrease in proliferation (p < 0.01) and an increase in apoptosis (p < 0.05). These results suggest that cancer cells with impaired mitochondrial function are more reliant on glycolysis for survival and proliferation. Targeting glycolysis in such contexts may offer a therapeutic advantage, highlighting the potential of metabolic interventions in cancer treatment.

Cancer Metabolism, Glycolysis Inhibition, Mitochondrial Dysfunction