Bioinformatics Analysis of LINC00917 Targets miR-3690/DDX39A Axis to Exacerbate Pancreatic Cancer Cell Growth Using Real-Time Quantitative Reverse Transcription PCR

Abstract

This study aims to reveal the effect of long intergenic non-protein coding RNA 917 (LINC00917) on pancreatic cancer (PC). Specifically, high expression of LINC00917 was validated in five PC cell lines. Colony formation, TUNEL, transwell, immunofluorescence staining and sphere formation assays were conducted in this research, and the results illustrated that LINC00917 accelerated PC cell proliferation, migration, EMT, but impaired the cell apoptosis. Moreover, a panel of mechanism assays were carried out to probe the involvement of LINC00917ceRNA mechanism. LINC00917 was corroborated to sequester miR-3690 to elevate DExD-box helicase 39A (DDX39A) expression. Additionally, the inhibition of miR-3690 on PC cell malignant phenotype was also demonstrated. We illustrated that LINC00917 promoted PC cell proliferation and inhibited the cell apoptosis. Furthermore, LINC00917 contributed to PC cell migration, EMT and stemness. The high enrichment of LINC00917 was detected in biotin-labeled wild-type miR-3690, indicating that LINC00917 bound miR-3690 at the predicted sites. We found that miR-3690 was sponged by LINC00917 and involved in LINC00917-mediated cell proliferation, apoptosis and migration. miR-3690 targeted DDX39A in PC cells, and DDX39A could completely rescue the functional effects of miR-3690. On the whole, DDX39A was required in LINC00917-mediated cell malignant behavior in PC cells. LINC00917 led to DDX39A increment and mediated PC cell biological functions through serving the miR-3690 sponge, indicating LINC00917 can be as a promising biomarker for PC.