MicroRNA-488 inhibits proliferation and glycolysis in human prostate cancer cells by regulating PFKFB3.
Jun WangXiaojuan LiZhaoming XiaoYu WangYuefu HanJun LiWeian ZhuQu LengYuehui WenXinqiao WenPublished in: FEBS open bio (2019)
Prostate cancer (PCa) remains the second leading cause of cancer-related death among men in the United States, and its molecular mechanism remains to be elucidated. Recent studies have suggested that microRNAs may play an important role in cancer development and progression. By analyzing the Gene Expression Omnibus dataset, we found lower expression for miR-488 in PCa than in normal tissues. Moreover, CCK-8, EdU, glucose uptake, and lactate secrete assays revealed that overexpression of miR-488 in PCa cell lines PC3 and DU145 resulted in inhibition of proliferation and glycolysis. In contrast, downregulation of miR-488 expression promoted proliferation and glycolysis in PCa cells. Using a bioinformatic approach and dual-luciferase reporter assays, we identified 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase, isoform3 (PFKFB3), as a direct target of miR-488. Inhibition of PFKFB3 also suppressed PCa cell glycolysis and proliferation. Our study suggests that miR-488 inhibits PCa cell proliferation and glycolysis by targeting PFKFB3, and thus, miR-488 may be a novel therapeutic candidate for PCa.
Keyphrases
- cell proliferation
- long non coding rna
- gene expression
- prostate cancer
- long noncoding rna
- poor prognosis
- cell cycle
- signaling pathway
- pi k akt
- endothelial cells
- high throughput
- dna methylation
- induced apoptosis
- computed tomography
- radical prostatectomy
- metabolic syndrome
- oxidative stress
- cell cycle arrest
- binding protein
- blood pressure
- cell death
- endoplasmic reticulum stress
- tyrosine kinase
- weight loss