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Linc01278 inhibits the development of papillary thyroid carcinoma by regulating miR-376c-3p/DNM3 axis

Authors Lin S, Tan L, Luo D, Peng X, Zhu Y, Li H

Received 31 May 2019

Accepted for publication 22 August 2019

Published 19 September 2019 Volume 2019:11 Pages 8557—8569


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Professor Bilikere Dwarakanath

Shaojian Lin,* Langping Tan,* Dingyuan Luo,* Xinzhi Peng, Yue Zhu, Honghao Li

Department of Thyroid Surgery, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou 510120, Guangdong, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Honghao Li
Department of Thyroid Surgery, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, No.107 of Yanjiangxi Road, Guangzhou 510120, Guangdong, People’s Republic of China

Purpose: Papillary thyroid carcinoma (PTC) is the most common endocrine malignancy, and its incidence has continuously increased in recent years. Therefore, it is essential to develop more useful therapeutic strategies.
Methods: We collected 56 pairs of PTC tissues and adjacent normal tissues and determined the expression patterns of linc01278, miR-376c-3p and DNM3. In addition, we analyzed the relationship between linc01278 expression and pathological information of PTC patients. Furthermore, the effects of linc01278, miR-376c-3p and DNM3 overexpression on proliferation, clonality, apoptosis, migration and invasion of PTC cell lines TPC1 and BCPAP were evaluated. The dual luciferase reporter assay was used to confirm the direct interaction between miR-376c-3p and linc01278.
Results: Linc01278 and DNM3 were remarkably down-regulated in PTC tissues and cell lines, whereas miR-376c-3p was significantly up-regulated. In addition, lower linc01278 expression was associated with increased tumor size, lymph node metastasis and higher clinical stage. Linc01278 inhibited cell proliferation of PTC cells by inducing apoptosis, and demonstrated attenuating effects on migration and invasion abilities of PTC cells by regulating the EMT process. More importantly, dual luciferase reporter experiments demonstrated the direct interaction between miR-376c-3p and linc01278, which revealed that DNM3 was a novel target of miR-376c-3p. The miR-376c-3p mimic significantly promoted the proliferation, migration and invasion of PTC cells, and inhibited cell apoptosis. Overexpression of DNM3 abolished the effects of the miR-376c-3p mimic on PTC cells. DNM3 expression was negatively correlated with miR-376c-3p expression, but was positively correlated with linc01278 expression.
Conclusion: Overall, we found that linc01278 can act as a competing endogenous RNA (ceRNA) to sponge miR-376c-3p, thereby positively regulating DNM3 expression and ultimately acting as a tumor suppressor gene in PTC progression.

Keywords: linc01278, papillary thyroid carcinoma, ceRNA, DNM3

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