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lncRNA SNHG14 promotes the proliferation, migration, and invasion of thyroid tumour cells by regulating miR-93-5p

Published online by Cambridge University Press:  12 August 2021

Fang Tian
Affiliation:
Department of Endocrinology, Hangzhou Xixi Hospital Affiliated to Zhejiang University of Traditional Chinese Medicine, Hangzhou, Zhejiang, China
Huimin Ying
Affiliation:
Department of Endocrinology, Hangzhou Xixi Hospital Affiliated to Zhejiang University of Traditional Chinese Medicine, Hangzhou, Zhejiang, China
Shuaiju Liao
Affiliation:
Department of Endocrinology, BenQ Medical Center, Nanjing, Jiangsu, China
Yuanyuan Wang
Affiliation:
Department of Endocrinology, Hangzhou Xixi Hospital Affiliated to Zhejiang University of Traditional Chinese Medicine, Hangzhou, Zhejiang, China
Quansheng Wang*
Affiliation:
Department of Endocrinology, BenQ Medical Center, Nanjing, Jiangsu, China
*
*Author for correspondence: Quansheng Wang, Department of Endocrinology, BenQ Medical Center, The Affiliated BenQ Hospital of Nanjing Medical University, 71 Hexi Street, Jianye District, Nanjing City, Jiangsu Province, 210019, China. E-mail: [email protected]

Summary

Long non-coding RNAs (lncRNAs) exert vital functions in the occurrence and development of various tumours. The aim of this study was to examine the regulatory effect and underlying molecular mechanism of lncRNA small nucleolar RNA host gene 14 (SNHG14) on the proliferation, invasion and migration of thyroid tumour cells. The expression of SNHG14 in thyroid tumour cell lines was determined using qRT-PCR. CCK-8 and western blot were used to detect the effects of SNHG14 on proliferation and apoptosis of thyroid tumour cells. The effect of SNHG14 on the migration and invasion of thyroid tumour cells was analyzed using immunofluorescence, wound-healing and transwell assays. A targeting relationship between SNHG14 and miR-93-5p was determined using bioinformatics software and luciferase reporter assays. In addition, CCK-8, immunofluorescence, wound-healing and transwell assays were applied to demonstrate that SNHG14 promoted the proliferation, migration and invasion of thyroid tumour cells by targeting miR-93-5p. The biological function of SNHG14 in vivo was explored through a xenograft model and immunohistochemistry. SNHG14 was upregulated in thyroid tumour cells compared with normal cells. Downregulation of SNHG14 effectively reduced the proliferation, migration and invasion of TPC-1 cells, and induced cell apoptosis. Moreover, SNHG14 directly targeted miR-93-5p and there was a negative correlation between them. Further functional experiments illustrated that miR-93-5p overexpression dramatically reversed the promoting role of SNHG14 in proliferation, migration and invasion of TPC-1 cells. Our results demonstrated that SNHG14 promotes the proliferation, invasion and migration of thyroid tumour cells by downregulating miR-93-5p.

Type
Research Article
Copyright
© The Author(s), 2021. Published by Cambridge University Press

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