LncRNA DCST1-AS1 was upregulated in endometrial carcinoma and may sponge miR-92a-3p to upregulate notch1

14Citations
Citations of this article
4Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

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 nega-tive 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, overexpres-sion 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.

Cite

CITATION STYLE

APA

Ke, J., Shen, Z., Hu, W., Li, M., Shi, Y., Xie, Z., & Wu, D. (2020). LncRNA DCST1-AS1 was upregulated in endometrial carcinoma and may sponge miR-92a-3p to upregulate notch1. Cancer Management and Research, 12, 1221–1227. https://doi.org/10.2147/CMAR.S234891

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free