Research Paper Volume 13, Issue 8 pp 12007—12015
LINC00514 promotes gastric cancer cell growth and EMT progression via miR-204-3p/KRAS
- 1 Pharmacy College of Ningxia Medical University, Yinchuan 750004, China
- 2 Ningxia Medical University Key Laboratory of Hui Ethnic Medicine Modernization Ministry of Education, Yinchuan 750004, China
- 3 Traditional Chinese Medicine College of Ningxia Medical University, Yinchuan 750004, China
- 4 Hepatobiliary Surgery, General Hospital of Ningxia Medical University, Yinchuan 750004, China
- 5 Department of Infectious Disease, The Fourth Hospital of Harbin Medical University, Harbin 150001, Heilongjiang, China
Received: October 9, 2020 Accepted: January 22, 2021 Published: April 22, 2021
https://doi.org/10.18632/aging.202905How to Cite
Copyright: © 2021 Yuan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Long noncoding RNAs (LncRNAs) participate in tumor development and tumorigenesis. However, the mechanism, function and expression of LINC00514 in GC remain unknown. We showed that LINC00514 was upregulated in GC specimens compared with nontumor specimens. Overexpression of LINC00514 induced cell growth and EMT progression in GC cells. By using bioinformatics prediction, we found that miR-204-3p contained binding sequences for LINC00514. Luciferase reporter analysis noted that miR-204-3p overexpression decreased the luciferase expression under LINC00514-wild-type and KRAS-wild-type reporters but not that under mutant reporter. Ectopic LINC00514 expression decreased miR-204-3p expression. miR-204-3p expression was decreased in GC specimens compared with nontumor specimens and that LINC00514 was negatively correlated with miR-204-3p in GC specimens. Furthermore, KRAS was identified as a target gene for miR-204-3p according to TargetScan. Elevated miR-204-3p expression inhibited KRAS expression in HGC-27 cells, and ectopic expression of LINC00514 enhanced KRAS expression. Elevated LINC00514 expression enhanced cell growth and EMT progression by sponging KRAS. Our data indicated that LINC00514 may act as an oncogene and therapeutic target for GC.