IL-37 regulates glycolysis by inhibiting GLUT1 expression in lung adenocarcinoma

Abstract Aerobic glycolysis is the most classical pathway in tumor metabolic reprogramming. Aerobic glycolysis has been found in several studies to have an essential role in lung adenocarcinoma progression. Interleukin 37 (IL-37) has an important protective role in lung cancer. The mechanism by which glycolysis in lung adenocarcinoma is affected by IL-37 has not been clarified. Using qRT-PCR and western blot, we uncovered that GLUT1 expression was significantly higher in A549 cells than in BEAS-2B cells. GLUT1 expression was decreased in A549 cells treated with rhIL-37. Also, glucose uptake and lactic acid production were significantly reduced in A549 cells treated with 6uM BAY-876 (GLUT1 specific inhibitor). GLUT1 expression in A549 cells in this study was not inhibited by intracellular overexpression of IL-37. Glucose uptake and lactic acid production may be inhibited by extracellular IL-37 by inhibiting GLUT1 expression. Therefore, IL-37 has a role in glucose metabolism in lung adenocarcinoma cells.