Research Paper Volume 11, Issue 19 pp 8139—8155
Hypermethylated long noncoding RNA MEG3 promotes the progression of gastric cancer
- 1 Department of Radiology, China-Japan Union Hospital of Jilin University, Changchun 130022, Jilin, China
- 2 Department of Medical Examination, China-Japan Union Hospital of Jilin University, Changchun 130022, Jilin,China
- 3 Department of Gynecology and Obstetrics, The Second Hospital of Jilin University, Changchun 130041, Jilin, China
- 4 Department of Ophthalmology, China-Japan Union Hospital of Jilin University, Changchun 130022, Jilin, China
- 5 Department of Ultrasonography, China-Japan Union Hospital of Jilin University, Changchun 130022, Jilin, China
- 6 Department of Colorectal and Anal Surgery, The First Hospital of Jilin University, Changchun 130000, Jilin, China
received: January 22, 2019 ; accepted: September 21, 2019 ; published: October 4, 2019 ;https://doi.org/10.18632/aging.102309
How to Cite
Copyright © 2019 Ding 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.
This study aims to explore the expression and degree of methylation of lncRNA MEG3 in gastric cancer tissues and to analyze its effect on the migration and proliferation of gastric cancer patients and the mechanism by which this occurs. The targeting relationship between MEG3, miR-181a-5p and ATP4B was detected through molecular biology experiments. Wound healing, transwell, colony formation and flow cytometry assays were used to analyze the effects of lncRNA MEG3 and methylation on tumor cell migration, invasion, proliferation and apoptosis. In addition, a tumor xenotransplantation model was established to study the influence of MEG3 on tumor growth in vivo. Bioinformatics analysis showed that lncRNA MEG3 and ATP4B were downregulated in gastric cancer tissues compared with normal tissues. Bioinformatics predicted that ATP4B might be regulated by targeting miR-181a-5p. The overexpression of MEG3 and the application of 5-Aza treatment inhibited the migration, invasion and proliferation of MGC-803 cells and promoted apoptosis. In gastric cancer tissues, MEG3 is hypermethylated to decrease expression. Once the expression of MEG3 is restored or methylation is inhibited, tumor growth can be inhibited both in vivo and in vitro. This finding could be utilized as a clinical reference for gastric cancer treatment in the future.
AML: acute myeloid leukemia; ANOVA: analysis of variance; CFR: clone formation rate; GC: gastric cancer; MEG3: maternally expressed gene 3; miR-181a-5p: MicroRNA-181a-5p; RPMI: Roswell Park Memorial Institute; RPMI1640: Roswell Park Memorial Institute1640.