GLUT1 expression in high-risk prostate cancer: correlation with 18 F-FDG-PET/CT and clinical outcome

Background Tumour 18 F-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 18 F-FDG-uptake on PET/CT imaging in PCa. Methods Retrospective analysis was conducted for 94 patients diagnosed with a Gleason sum ≥8 adenocarcinoma of the prostate at biopsy between July 2011 and July 2014 who underwent 18 F-FDG-PET/CT imaging before radical prostatectomy (RP). 18 F-FDG-uptake in primary lesion was measured by a blinded reader using maximum standardised uptake value (SUV max ). GLUT1, GLUT12 and HK2 expression were blindly scored after immunohistochemistry on specimens RP by three pathologists. Correlations between GLUT1, GLUT12 and HK2, and SUV max 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 (BCR), 7% ( n = 7) progressed to castration-resistant prostate cancer (CRPC) disease, 13% ( n = 12) developed metastasis and 6% ( n = 6) died. Correlation was found between GLUT1 expression and SUVmax level ( r = 0.25, p = 0.02). In addition, SUV max 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 = 0.004). Moreover, a significant association was found between GLUT1 expression levels and SUV max level ( p = 0.005), lymph node status ( p = 0.05), volume of cancer ( p = 0.01), CRPC disease progression ( p = 0.02) and metastasis development ( p = 0.04). No significant difference between GLUT12 and HEX2 expression and SUV max have been found. Conclusions GLUT1 expression in PCa tumours correlates with 18 F-FDG-uptake and poor prognostic factors. These results suggest that this transporter is involved in the molecular mechanism of 18 F-FDG-uptake in high-risk PCa and raise interest in targeting metabolic dependencies of PCa cells as a selective anticancer strategy.