Abstract
Increasing evidence indicates that long non-coding RNAs (lncRNAs) are associated with the progression of human cancers. However, the expression level and function of LINC01559 (long intergenic non-protein coding RNA 1559) in gastric cancer (GC) are rarely reported. Here we found that LINC01559 was upregulated in GC tissues based on GEPIA (Gene Expression Profiling Interactive Analysis) and TCGA (The Cancer Genome Atlas) databases. Also, LINC01559 was expressed at a lower level in GC cells than in mesenchymal stem cells (MSCs). In vitro experiments revealed that silencing LINC01559 remarkably hindered GC cell proliferation, migration and stemness. Then, we identified that LINC01559 was transmitted form MSCs to GC cells via the exosomes. Immunofluorescence staining and electron microscope validated the existence of exosomes in GC cells. Mechanistically, LINC01559 sponged miR-1343-3p to upregulate PGK1 (phosphoglycerate kinase 1), therefore activating PI3K/AKT pathway. Moreover, LINC01559 recruited EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit) to PTEN (phosphatase and tensin homolog) promoter, inducing the methylation of PTEN promoter and finally resulting in PTEN repression. Of note, LINC01559 targeted both PGK1 and PTEN to promote GC progression by activating PI3K/AKT pathway. Taken together, our study demonstrated that LINC01559 accelerated GC progression via upregulating PGK1 and downregulating PTEN to trigger phosphatidylinositol 3-kinase/AKT serine/threonine kinase (PI3K/AKT) pathway, indicating LINC01559 as a potential biomarker for GC treatment.
Highlights
Gastric cancer (GC) is a well-known gastrointestinal tumor with high morbidity around the world[1]
Cancer-pku.cn) and The Cancer Genome Atlas (TCGA), we unveiled that the expression of LINC01559, LINC00483, LINC01296, RAET1E-AS1 and PCED1B-AS1 was significantly high in STAD tissues in contrast with normal gastric tissues (Fig. 1a, Supplementary Fig. 1A)
Compared to mesenchymal stem cells (MSCs), only LINC01559 presented a relatively low level in GC cells, while the expression of other 4 long non-coding RNAs (lncRNAs) exhibited no statistical differences between these two kinds of cells (Fig. 1b, Supplementary Fig. 1B)
Summary
Gastric cancer (GC) is a well-known gastrointestinal tumor with high morbidity around the world[1]. Many factors are responsible for triggering GC such as heavy drinking, irregular dieting, unscientific dieting habit and genetic inheritance[2,3]. Traditional treatments for patients with GC include chemotherapy and surgery. More and more attention has been paid to molecular targeted therapy. The types and efficacy of targeted drugs for GC are limited[4]. It is necessary to find out new and efficient biomarkers for GC treatment
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