Back to Journals » Cancer Management and Research » Volume 12

LncRNA DCST1-AS1 Was Upregulated in Endometrial Carcinoma and May Sponge miR-92a-3p to Upregulate Notch1

Authors Ke J, Shen Z, Hu W, Li M, Shi Y, Xie Z, Wu D

Received 16 October 2019

Accepted for publication 6 January 2020

Published 18 February 2020 Volume 2020:12 Pages 1221—1227

DOI https://doi.org/10.2147/CMAR.S234891

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Professor Bilikere Dwarakanath


Jieqi Ke, Zheng Shen, Weiping Hu, Min Li, Yangyang Shi, Zhen Xie, Dabao Wu

Department of Obstetrics and Gynecology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001, People’s Republic of China

Correspondence: Dabao Wu
Department of Obstetrics and Gynecology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001, People’s Republic of China
Tel +86-551-62283954
Email ia0940@163.com

Introduction: The functions of DCST1-AS1 have been investigated in liver cancer, while its role in endometrial carcinoma (EC) remains hardly known. This study aimed to analyze the role of DCST1-AS1 in EC.
Methods: Paired EC and non-tumor tissue samples were obtained from 62 EC patients. These patients were followed up for 5 years since their admission to record their survival conditions. HEC-1 cells were transfected with DCST1-AS1, Notch1 vectors, miRNA negative control or miR-92a-3p mimic. Luciferase activity was measured. QPCR and Western blot were applied to determine the RNA level and protein expression, respectively. The invasion and migration of HEC-1 cells were analyzed by Transwell assay.
Results: We in this study found that DCST1-AS1 was upregulated in EC. Survival analysis revealed that high levels of DCST1-AS1 expression predicted poor survival of EC patients. Bioinformatics analysis revealed that miR-92a-3p may bind DCST1-AS1 and the interaction between them was further confirmed by dual-luciferase activity assay. However, overexpression of miR-92a-3p and DCST1-AS1 failed to affect the expression of each other. Moreover, DCST1-AS1 overexpression led to upregulated Notch1 and increased cancer cell invasion and migration rates. Overexpression of miR-92a-3p played an opposite role and attenuated the effects of DCST1-AS1 overexpression.
Discussion: DCST1-AS1 is downregulated in EC and may sponge miR-92a-3p, thereby promoting cancer cell invasion and migration.

Keywords: endometrial carcinoma, DCST1-AS1, miR-92a-3p, Notch1

Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Download Article [PDF]  View Full Text [HTML][Machine readable]