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LncRNA SNHG16 drives proliferation and invasion of papillary thyroid cancer through modulation of miR-497

Authors Wen Q, Zhao L, Wang T, Lv N, Cheng X, Zhang G, Bai L

Received 8 September 2018

Accepted for publication 13 December 2018

Published 18 January 2019 Volume 2019:12 Pages 699—708


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Manfred Beleut

Peer reviewer comments 3

Editor who approved publication: Dr Federico Perche

Qiang Wen,1,* Lina Zhao,2,* Tongtong Wang,1 Ningning Lv,1 Xuejiao Cheng,1 Guang Zhang,2 Lin Bai1

1Department of Nuclear Medicine, China-Japan Union Hospital of Jilin University, ErDao District, Changchun 13033, China; 2Department of Thyroid Surgery, China-Japan Union Hospital of Jilin University, ErDao District, Changchun 13033, China

*These authors contributed equally to this work

Background: Long noncoding small nucleolar RNA host gene 16 (SNHG16) has been shown to play an oncogenic role in multiple cancers. However, the biological roles and mechanism of SNHG16 action in the regulation of papillary thyroid cancer (PTC) remains unknown. The aims of this study were to investigate the roles and the possible mechanism of SNHG16 in PTC progression.
Materials and methods: The expression of SNHG16 PTC tissues and cell lines was detected by reverse-transcription quantitative PCR (qRT-PCR). The effect of SNHG16 on cell proliferation, apoptosis, migration, and invasion was detected by Cell Counting Kit-8, flow cytometry, wound-healing assay, and Matrigel invasion assay, respectively. In addition, the regulatory relationships between SNHG16 and miR-497 were explored by luciferase reporter assay and qRT-PCR.
Results: The SNHG16 expression was upregulated in PTC tissues and cell lines, whose expression was positively associated with advanced TNM stage and lymph node metastasis. Function analysis demonstrated that depletion of SNHG16 in PTC cells significantly inhibited cell proliferation, induced cell apoptosis, and suppressed cell migration and invasion abilities. Mechanistic studies indicated that SNHG16 functioned as an endogenous sponge for miR-497 to regulate its target genes brain-derived neurotrophic factor and yes-associated protein 1 expression. Furthermore, the inhibition of miR-497 antagonized the suppressive effect of SNHG16-depleted cells on cell proliferation, migration, and invasion.
Conclusion: These findings revealed that SNHG16 drived the PTC progression possibly via regulating miR-497, suggesting that SNHG16 might be a novel therapeutic agent for PTC.

Keywords: papillary thyroid cancer, long noncoding RNAs, SNHG16, miR-497

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