Artemisinin suppresses aerobic glycolysis in thyroid cancer cells by downregulating HIF-1a, which is increased by the XIST/miR-93/HIF-1a pathway.

Abstract

The incidence of thyroid cancer (TC) continues to increase worldwide. Aerobic glycolysis, the prominent feature of glucose metabolism in cancer progression, is associated with TC. We first demonstrated that HIF-1a is highly expressed in TC tissues and is positively correlated with the level of XIST in the serum of patients with TC. Then, we proved that XIST regulates the expression of HIF-1a through the XIST/miR-93/HIF-1a pathway, thereby regulating the level of glycolysis in TC cells. Knockdown of XIST inhibits glycolysis, proliferation, the cell cycle and metastasis of TC cells. Finally, we verified that artemisinin could target the degradation of HIF-1a and inhibit glycolysis in TC cells. Collectively, XIST levels in serum may be used as a tumor marker for TC promoted by HIF-1a, which could be treated using artemisinin.