Abstract
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.
Highlights
As a typical malignancy, gastric cancer (GC) remains the third most widely common cancer and has resulted in an increasing huge number of deaths worldwide [1, 2]
LncRNA maternally expressed gene 3 (MEG3) and ATP4B were downregulated in gastric cancer tissues
All the results suggested that MEG3 and ATP4B were downregulated in GC patients
Summary
Gastric cancer (GC) remains the third most widely common cancer and has resulted in an increasing huge number of deaths worldwide [1, 2]. As the Asian population is aging, the number of elderly patients with this disease is increasing [4]. Due to this fact, a more comprehensive and profound understanding of GC is urgently needed to discover an optimized and efficient diagnostic strategy to prevent and treat gastric cancer at an early stage [3]. DNA methylation is widely studied in various fields of diseases It regulates the expression of various genes, especially those related to cancer, and tumors usually reflect distinctive patterns of DNA methylation [5]. The abundance of abnormal DNA methylation in gastric mucosae, mostly induced by H. pylori infection, is strongly related to a predisposition to gastric cancers [8]
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