The SP1/SNHG16/GLUT1 axis promotes prostate cancer proliferation and invasion by regulating glucose metabolism

Introduction The SP1/SNHG16/GLUT1 is involved in diverse cancer-related process. This study was designed to study the role of SP1/SNHG16/GLUT1 axis in prostate cancer (PCa) via modulation of glucose metabolism. Material and methods The expression profile of SNHG16 in PCa tissues was obtained from the online public database GEPIA (http://gepia.cancer-pku.cn/). Real-time qPCR was used to ascertain the mRNA expression. To find cellular proliferation and invasion, respectively, CCK-8, transwell, and glycolysis were used to monitor proliferation, invasion, and glycolysis. Results Analysis of GEPIA2 data revealed upregulation of SNHG16 in PCa tissues and a positive association between GLUT1 (SLC2A1) and SP1/SNHG16 expression in the correlation study. Consistently, SPI and SNHG16 were either overexpressed or knocked down in PCa cells to unveil the role of the SP1/SNHG16/GLUT1 axis. Results demonstrated that PC-3 and DU145 cell proliferation were promoted by the overexpression of either SPI or SNHG16. On the other hand, PC-3 and DU145 cell proliferation were reduced upon knockdown of SP1 or SNHG16. A real-time qPCR study revealed that GLUT1 mRNA was upregulated by SP1/SNHG16 overexpression and downregulated by SP1/SNHG16 knockdown. In PCa cells, overexpression of SNHG16/SP1 resulted in enhanced utilization of glucose, lactose, and ATP production, whereas SNHG16/SP1 knockdown had the reverse effect. Lastly, transwell assay results showed that overexpression of SNHG16/SP1 promoted, while knockdown of SNHG16/SP1 inhibited the invasiveness of PC-3 and DU145 PCa cells. Conclusions Collectively, the SP1/SNHG16/GLUT1 axis regulates the proliferation of PCa cells via the glycolytic route and thus may act as a therapeutic target for PCa treatment.