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MiR-153-3p Suppresses Cell Proliferation, Invasion and Glycolysis of Thyroid Cancer Through Inhibiting E3F3 Expression

Authors Deng X, Guo B, Fan Y

Received 15 June 2020

Accepted for publication 11 November 2020

Published 18 January 2021 Volume 2021:14 Pages 519—529

DOI https://doi.org/10.2147/OTT.S267887

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Federico Perche


Xianzhao Deng, Bomin Guo, Youben Fan

Department of General Surgery, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, Shanghai 200233, People’s Republic of China

Correspondence: Youben Fan
Department of General Surgery, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, 600 Yishan Road, Shanghai 200233, People’s Republic of China
Tel +86-21-24058410
Email dryouben_f123@163.com

Purpose: The aim was to research the role of miR-153-3p and E2F3 in the development of thyroid tumors.
Methods: A total of 91 thyroid cancer patients were involved. The role of miR-153-3p in THCA cell lines and Nthy-ori3-1 cell line was researched. qPCR was used to detect miR-153-3p and E2F3 expression. MiR-153-3p mimic, inhibitor, siE2F3 or corresponding controls were transfected in cells. CCK8 was used to verify the proliferation. Cell cycle and apoptosis was detected by flow cytometry. Transwell assay was applied for migration and invasion, and glycolysis was monitored. The binding of miR-153-3p and E2F3 was predicted by targetscan database, and verified by luciferase reporter and RNA-pull down assay. Western blot was used to detect E2F3 expression. Rescue assay was undertaken to verify the effect of siE2F3 on miR-153-3p inhibitor. Moreover, the effect of miR-153-3p mimic on tumor volume and weight was measured. IHC assay was processed to E2F3 and Ki67 expression, and TUNEL assay was used for apoptosis.
Results: MiR-153-3p expressed lower in thyroid tumors and cells. The level of miR-153-3p was negatively related with TNM stage. MiR-153-3p inhibited cell proliferation, invasion migration, and induced cycle arrest and apoptosis. Moreover, it negatively regulated E2F3. siE2F3 rescued effects of miR-153-3p inhibitor in all above biological processes in thyroid cancer cells. MiR-153-3p inhibited tumor growth. Moreover, it inhibited E2F3 and Ki67 expression, and also increased apoptosis in vivo.
Conclusion: MiR-153-3p suppresses cell proliferation, invasion and glycolysis of thyroid cancer through inhibiting E3F3 expression, which may be a biomarker for thyroid cancer diagnose.

Keywords: thyroid cancer, MiR-153-3p, E3F3, proliferation, invasion, glycolysis

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