Metastasis is a major dilemma of cancer therapy. It frequently occurs in breast cancer, which is the leading form of malignant tumor among females worldwide. Although there are therapies that provide a possible method for this challenge, such as chemotherapy, the tumoral metabolic pathway is unconventional and favors metastasis and proliferation. This magnifies the difficulty of treating breast cancer. In this study, we identified 2-deoxyglucose (2 DG) as an important glycolysis suppressor that can potentiate sonodynamic therapy (SDT) to inhibit migration and invasion. In addition, disruptions of the cell membrane microstructure were captured by a scanning electron microscope in cells treated with the co-therapy. Similarly, we detected blockages of the cell cycle process, using flow cytometry. Of note, we observed that hexokinase II (HK2), the rate-limiting enzyme of glycolysis, was notably uncoupled from the mitochondria in SDT + 2 DG co-therapy group. Furthermore, there was altered expression of HK2 and Glut1, which control glycolysis. Simultaneously, the in vivo results revealed that pulmonary metastasis was also seriously suppressed by SDT + 2 DG co-therapy. These results demonstrate this co-therapy is a promising strategy for breast cancer inhibition through metastasis and proliferation.
Keywords: 2-Deoxyglucose; Breast cancer; Metastasis; Proliferation; Sonodynamic therapy.
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