MiR-26b-5p Downregulates Proliferation and Invasion of PANC-1 Cell via MKNK2/eIF4E Signal Pathway
WANG Yue-hua，ZENG Li-ping，ZENG Jiu-ping
Abstract:
Objective To screen out the microRNA associated with pancreatic cancer (PC) progression and validate its biological functions, target genes and potential signal pathways. Methods We performed differential analysis for miR-26b-5p, based on the GSE71533 and the GSE85589 datasets from Gene Expression Omnibus. Then, Kaplan-Meier survival analysis was conducted to evaluate the influence of miR-26b-5p on PC patients' overall survival based on the PC cohort of The Cancer Genome Atlas (TCGA). The TargetScan database was used to predict the target genes of miR-26b-5p and the Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted to reveal the functions of the miR-26b-5p targeting gene set. in vitro and Western blotting assays were performed to validate the influence of miR-26b-5p on PANC-1 cell progression and to identify the target gene of miR-26b-5p. Results In GSE71533, miR-26b-5p was downregulated in PC tissues compared with normal tissues (9.65±0.10 vs 10.18±0.07，P<0.001). In GSE85589, miR-26b-5p was downregulated in PC patients' serum (0.67±0.18 vs 0.79±0.24，P=0.017). Downregulation of miR-26 b-5 p was associated with the poor overall survival in the PC cohort of showed that miR-26b-5p suppressed PANC-1 cell proliferation, migration and invasion. Western blotting assays suggested that miR-26b-5p downregulated MKNK2 and the downstream gene eIF4E. Conclusion The miR-26b-5p suppressed PANC-1 cell proliferation and invasion via MKNK2/eIF4E. The miR-26b-5p could serve as apotential biomarker for PC diagnosis and a target for PC treatment.
