Therapeutic role of EF 24 targeting glucose transporter 1‐mediated metabolism and metastasis in ovarian cancer cells

Cancer cells require glucose to support their rapid growth through a process known as aerobic glycolysis, or the W arburg effect. As in ovarian cancer cells, increased metabolic activity and glucose concentration has been linked to aggressiveness of cancer. However, it is unclear as to whether targeting the glycolytic pathway may kill the malignant cells and likely have broad therapeutic implications against ovarian cancer metastasis. In the present research, we found that EF 24, a HIF ‐1α inhibitor, could significantly block glucose uptake, the rate of glycolysis, and lactate production compared with vehicle treatment in SKOV ‐3, A 2780 and OVCAR ‐3 cells. These results might possibly contribute to the further observation that EF 24 could inhibit ovarian cancer cell migration and invasion from wound healing and Transwell assays. Furthermore, as an important mediator of glucose metabolism, glucose transporter 1 ( G lut1) was found to contribute to the function of EF 24 in both energy metabolism and metastasis. To examine the effect of EF 24 and the mediated role of G lut1 in vivo in a xenograph subcutaneous tumor model, intraperitoneal metastasis and lung metastasis model were introduced. Our results indicated that EF 24 treatment could inhibit tumor growth, intraperitoneal metastasis and lung metastasis of SKOV ‐3 cells, and G lut1 is a possible mediator for the role of EF 24. In conclusion, our results highlight that an anti‐cancer reagent with an inhibiting effect on energy metabolism could inhibit metastasis, and EF 24 is a possible candidate for anti‐metastasis therapeutic applications for ovarian cancer.