BIOLOGY MOLECULAR / RESEARCH PAPER
The SP1/SNHG16/GLUT1 axis promotes prostate cancer proliferation and invasion by regulating glucose metabolism
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1
Department of Urology, The First Affiliated Hospital and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, Henan 471000,, China
2
Department of General Practice, The First Affiliated Hospital and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, Henan 471000,, China
Submission date: 2024-01-30
Final revision date: 2024-07-02
Acceptance date: 2024-07-12
Online publication date: 2024-07-28
Corresponding author
Hua Huang
Department of Urology, The First Affiliated Hospital and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, Henan 471000,, 471000, Luoyang, China
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ABSTRACT
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.