291 Background: Tumour FDG-uptake is of prognostic value in high-risk and metastatic prostate cancer (PCa). The aim of this study is to investigate the underlying glucose metabolism mechanisms of 18F-FDG-uptake on PET/CT imaging in PCa. Methods: Retrospective analysis was conducted for 94 patients diagnosed with a Gleason sum ≥8 at biopsy who underwent 18F-FDG-PET/CT imaging before radical prostatectomy. GLUT1, GLUT12 and HK2 expression were blindly scored after immunohistochemistry on radical prostatectomy specimens by 3 pathologists. 18F-FDG-uptake in primary lesion was measured by a blinded reader using maximum standardized uptake value (SUVmax). Correlations between GLUT1, GLUT12 and HK2 and SUVmax were assessed using Spearman’s rank correlation test. Survival probabilities were based on the Kaplan-Meier method. Results: With a median follow-up of 4.5 years, 56% (n=53) of patients had biochemical recurrence, 7% (n=7) progressed to castration-resistant PCa (CRPC) disease, 13% (n=12) developed metastasis and 6% (n=6) died. Correlation was found between GLUT1 expression and SUVmax level (r=0.2512, p=0.0182). In addition, SUVmax was significantly higher in tumours with high GLUT1 expression (n=17, 5.74±1.67) than tumours with low GLUT1 expression (n=71, 2.68±0.31, P=0.0037). Also, contrary to GLUT12 and HEX2 expression, a significant association was found between GLUT-1 expression levels and SUVmax index (p=0.004), lymph node status (p=0.046), volume of cancer (P=0.013), CRPC-free survival (p=0.02) and metastasis-free survival (p=0.04). Conclusions: GLUT1 expression in PCa tumours correlates with 18F-FDG-uptake and poor prognostic factors. These results suggest that this transporter is involved in the molecular mechanism of 18F-FDG-uptake in high-risk PCa and raise interest in targeting metabolic dependencies of PCa cells as a selective anticancer strategy.