Objective: Aberrantly expressed lncRNAs have been detected in gastric cancer (GC). LncRNA is involved in numerous types of human malignant tumor. In this project, we demonstrated the relationship between and and tested the function of and hsa-miR-30a-3p in the tumorigenesis of GC.

Methods: For experimental study, RNA-Seq datasets and equivalent clinical data for 367 samples were achieved from The Cancer Genome Atlas (TCGA)-STAD datasets. The online software clusterProfiler was used to perform Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway functional enrichment. The co-expression of , , and genes was evaluated by determining the Pearson correlation coefficients. Potential competing endogenous RNAs of -miRNA- were predicted by the Cytoscape tool and Kaplan- Meier curves were generated for , , and genes. For clinical study, Human GC samples were taken from 26 pairs of GC tissue (GCT) and para-tumor tissue (PT, 5 cm from the edge of the tumor) in which no patient had previously undergone preoperative adjuvant chemotherapy or radiotherapy.

Results: For experimental study, a total of 1144 differential expression genes (DEGs) were identified consisting of 731 up-regulated genes and 413 down-regulated genes. DEGs were , , and and was significantly different (adj. =1.11E-11). The correlation coefficient between and was 0.42. A ceRNA network model suggested the hsa-miR-30a-3p was interacted between and , playing the role of information transmission. Survival analysis of these genes suggested that lncRNA might influence the GC case survival (=0.06). expression was upregulated in human gastric cancer tissues and its relative expression of PT was increased two fold compared to GCT. The expressions of from the tumor tissues were significantly upregulated in GCT.

Conclusion: These discoveries imply that lncRNA and hsa-miR-30a-3p has a responsibility in the GC development. Therefore, targeting or/and hsa-miR-30a-3p as a strategy for gastric cancer should be explored.

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