Altered expression of DLG1-AS1 distinguished papillary thyroid carcinoma from benign thyroid nodules

Abstract Background Benign thyroid nodules (BTN) are frequently diagnosed as papillary thyroid carcinoma (PTC), leading to unnecessary treatment. We found that plasma lncRNA DLG1-AS1 was upregulated in PTC patients but not in BTN patients and healthy controls. Methods In this study DLG1-AS1 and miR-...

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Bibliographic Details
Main Authors: Tao He, Huan Wang, Jiangming Sun, Jie Wu, Fakuo Gong, Shujun Li, Hui Wang, Yufeng Li
Format: Article
Language:English
Published: BMC 2019-11-01
Series:BMC Endocrine Disorders
Subjects:
Online Access:http://link.springer.com/article/10.1186/s12902-019-0440-x
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Summary:Abstract Background Benign thyroid nodules (BTN) are frequently diagnosed as papillary thyroid carcinoma (PTC), leading to unnecessary treatment. We found that plasma lncRNA DLG1-AS1 was upregulated in PTC patients but not in BTN patients and healthy controls. Methods In this study DLG1-AS1 and miR-199a-3p in plasma of both PTC patients and BTN patients were detected by qPCR. ROC curve analysis was performed for diagnostic analysis. Overexpression experiments were performed to analyze the interaction between DLG1-AS1 and miR-199a-3p. CCK-8 assay was performed to analyze cell proliferation. Results In this study, upregulation of DLG1-AS1 distinguished PTC patients from BTN patients and healthy controls. Plasma miR-199a-3p was downregulated in PTC patients compared with healthy controls and BTN patients. Plasma levels of miR-199a-3p were inversely correlated in PTC patients, but not in BTN patients and healthy controls. miR-199a-3p overexpression failed to significantly affect DLG1-AS1, while DLG1-AS1 overexpression resulted in downregulated miR-199a-3p, In addition, DLG1-AS1 overexpression promoted the proliferation of PTC cells. miR-199a-3p overexpression played an opposite role and attenuated the effects of DLG1-AS1 overexpression. Conclusions Therefore, DLG1-AS1 may promote PTC by downregulating miR-199a-3p.
ISSN:1472-6823