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Published in: BMC Endocrine Disorders 1/2019

Open Access 01-12-2019 | Research article

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

Authors: Tao He, Huan Wang, Jiangming Sun, Jie Wu, Fakuo Gong, Shujun Li, Hui Wang, Yufeng Li

Published in: BMC Endocrine Disorders | Issue 1/2019

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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.
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Metadata
Title
Altered expression of DLG1-AS1 distinguished papillary thyroid carcinoma from benign thyroid nodules
Authors
Tao He
Huan Wang
Jiangming Sun
Jie Wu
Fakuo Gong
Shujun Li
Hui Wang
Yufeng Li
Publication date
01-12-2019
Publisher
BioMed Central
Published in
BMC Endocrine Disorders / Issue 1/2019
Electronic ISSN: 1472-6823
DOI
https://doi.org/10.1186/s12902-019-0440-x

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