¹⁸F-fluorodeoxyglucose uptake predicts MET expression in lung adenocarcinoma

MET is a member of the receptor tyrosine kinases. Several MET-targeting inhibitors and antagonistic antibodies have shown promising data in clinical trials of lung adenocarcinoma. Finding noninvasive diagnostic tools to estimate the status of MET is helpful in clinical practice. ¹⁸F-fluorodeoxyglucose positron emission tomography/computerized tomography (¹⁸F-FDG PET/CT) has been used routinely for the diagnosis and staging of tumors. However, the relationship between MET expression and ¹⁸F-FDG uptake has not been investigated yet. This study aimed to determine the correlation of MET expression with ¹⁸F-FDG uptake on PET-CT scan and whether or not ¹⁸F-FDG PET/CT can be used to predict the MET status of lung adenocarcinoma patients.

Fifty-seven lung adenocarcinoma patients were analyzed in our study. Maximum standardized uptake value (SUV_max) was calculated in all PET/CT images. The expression levels of MET and two important glycolysis-related markers, glucose transporter 1 (GLUT1) and pyruvate kinase M2, were analyzed by immunohistochemistry of tissues. Spearman rank correlation was used to analyze the association between MET expression and SUV_max. In vitro MET knockdown in lung adenocarcinoma cells was used to examine the role of MET in tumor metabolism. The effect of MET on GLUT1 expression was investigated using Western blot assay and quantitative polymerase chain reaction.

SUV_max was positively correlated with the expression levels of MET (r=0.458; P<0.001) and GLUT1 (r=0.551; P<0.001). SUV_max was significantly higher in patients with positive MET expression than in those with negative MET expression (9.92±6.62 vs 4.60±3.00; P=0.002). MET knockdown in lung adenocarcinoma cells led to a significant decrease in GLUT1 expression and ¹⁸F-FDG uptake.

MET could increase ¹⁸F-FDG uptake by upregulating GLUT1 expression. ¹⁸F-FDG PET/CT could be used to predict the MET status of lung adenocarcinoma patients and to supply valuable information to guide targeted therapy.