Clinical significance of miR-34a expression in thyroid diseases – an 18F-FDG PET-CT study
Authors Chen L, Yang C, Feng J, Liu X, Tian Y, Zhao L, Xie R, Liu C, Zhao S, Sun H
Received 2 June 2017
Accepted for publication 14 November 2017
Published 15 December 2017 Volume 2017:9 Pages 903—913
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Akshita Wason
Peer reviewer comments 3
Editor who approved publication: Professor Nakshatri
Long Chen,1,* Conghui Yang,1,* Jun Feng,2,* Xin Liu,3,* Yadong Tian,1 Lei Zhao,1 Ran Xie,1 Chao Liu,4 Sheng Zhao,1 Hua Sun1
1Department of PET/CT Center, 2Department of Radiology, 3Department of Pathology, 4Department of Nuclear Medicine, Yunnan Tumor Hospital, The Third Affiliated Hospital of Kunming Medical University, Kunming, People’s Republic of China
*These authors contributed equally to this work
Purpose: To evaluate the possible roles of miR-34a expression in thyroid lesions, to unravel the correlation between fluorodeoxyglucose (FDG) uptake and miR-34a expression and moreover, to discover the underlying mechanisms by which miR-34a regulates FDG avidity.
Methods: We retrospectively reviewed 75 patients with pathology-confirmed thyroid diseases who underwent 18F-FDG positron emission tomography/computed tomography (PET/CT) within 3 months before undergoing thyroid surgery and miR-34a analysis from June 2012 to July 2017. 18F-FDG uptake of thyroid lesions was also analyzed semiquantitatively using maximum standardized uptake value (SUVmax). The association between miR-34a expression and clinicopathological variables (age, sex, TNM stage, histopathology, lesion numbers, location and 18F-FDG avidity) was investigated. When there were multiple lesions in thyroid bed, only the one with the highest 18F-FDG uptake was analyzed. Next, we inhibited the miR-34a expression in TPC-1 cells and detected the expression of glucose transporter 1 (GLUT1) mRNA and protein.
Results: In the patients cohort, miR-34a was upregulated in those with malignant thyroid diseases compared with benign lesions. The expression of miR-34a was associated with tumor stages, histopathological types and SUVmax. There was an inverse relationship between miR-34a expression and SUVmax in patients with thyroid diseases (Spearman correlation coefficient = –0.553, P < 0.0001). With an SUVmax of 4.3 as the threshold, sensitivity and specificity of the prediction of miR-34a expression (low or high) were 70% and 94.3%, respectively. The area under the receiver operating characteristic curve was 0.843 (95% confidence interval: 0.749, 0.936; P = 0.001). Inhibiting miR-34a in TPC-1 cells significantly increased GLUT1 mRNA and protein expression.
Conclusion: miR-34a expression was upregulated in thyroid lesions, negatively correlated with SUVmax and can be predicted by FDG SUVmax. In addition, miR-34a may regulate FDG avidity via targeting GLUT1.
Keywords: miR-34a, thyroid cancer, PET/CT
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