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Knockdown of lncRNA TDRG1 Inhibits Tumorigenesis in Endometrial Carcinoma Through the PI3K/AKT/mTOR Pathway

Authors Sun R, Sun X, Liu H, Li P

Received 21 August 2019

Accepted for publication 21 November 2019

Published 11 December 2019 Volume 2019:12 Pages 10863—10872

DOI https://doi.org/10.2147/OTT.S228168

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Prof. Dr. Geoffrey Pietersz


Ruimei Sun,1 Xiujiang Sun,2 Hua Liu,3 Peirui Li2

1Department of Radiotherapy, The Affiliated Hospital of Weifang Medical University, Weifang 261041, People’s Republic of China; 2Department of Thyroid and Breast Surgery, The Affiliated Hospital of Weifang Medical University, Weifang 261041, People’s Republic of China; 3Department of Gynaecology, The Affiliated Hospital of Weifang Medical University, Weifang 261041, People’s Republic of China

Correspondence: Peirui Li
Department of Thyroid and Breast Surgery, The Affiliated Hospital of Weifang Medical University, No. 2428, Yuhe Road, Weifang 261041, People’s Republic of China
Tel +86-0536-3081399
Email lipeirui536@sina.com

Background and objective: Endometrial carcinoma (EC) is one of the most frequently diagnosed malignancies in females. Dysregulation of lncRNA TDRG1 has been widely documented in several cancers, including EC. However, the mechanism of this lncRNA involving in EC progression remains to be further elucidated.
Materials and methods: The enrichment levels of TDRG1 in EC tissues and cell lines were examined by RT-qPCR. Flow cytometry, cell counting kit-8 (CCK-8), transwell, and Western blot assays were conducted to assess whether TDRG1 knockdown could affect cell cycle arrest, proliferation, migration, invasion, and apoptosis of EC cells. The phosphorylation levels of mTOR, AKT and PI3K that associated with PI3K/Akt/mTOR pathway were determined by Western blot assay.
Results: TDRG1 expression was markedly upregulated in EC tissues and cell lines. Knockdown of TDRG1 significantly induced cell cycle arrest and apoptosis, inhibited cell proliferation, restrained the invasion and migration abilities in EC cells. Moreover, TDRG1 silencing decreased the protein levels of p-AKT, p-PI3K, and p-mTOR of EC cells.
Conclusion: Our data underlined the implication of TDRG1 in EC progression, proposing that targeting TDRG1 might be a potential therapeutic avenue in EC.

Keywords: endometrial carcinoma, TDRG1, PI3K/AKT/mTOR pathway

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