Abstract
Barasertib is a highly selective Aurora kinase B (AURKB) inhibitor and has been widely applied in a variety of cancer cells to investigate the regulatory function of AURKB. However, the effect of barasertib on glucose metabolism in gastric cancer (GC) remains illustrated. Here, barasertib was identified to effectively reduce glucose uptake and lactate production in GC cells in a dose-dependent and time-dependent manner. The expression levels of GLUT1, LDHA and HK2 were decreased by barasertib treatment of GC cells. Furthermore, we found that barasertib induced the expression of ribosomal protein S7 (RPS7), as a tumor suppressor, to regulate glucose metabolism. Silencing of RPS7 rescued the effects of barasertib on glucose metabolism in GC cells. Overexpression of RPS7 suppressed the promoter activity of C-Myc, which has been identified as an important regulator of glucose metabolism in cancer cells. The clinical data showed that the expression level of AURKB in GC patients' sera and tissues were positively correlated with those of C-Myc, GLUT1 and LDHA, but negatively with that of RPS7. Therefore, these findings provide new evidence that barasertib regulates GC cell glucose metabolism by inducing the RPS7/C-Myc signal pathway, and have important implications for the development of therapeutic approaches using AURKB as a target protein to prevent tumor recurrence.
Published Version
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