MiR‐766‐3p Inhibit the Proliferation, Stemness, and Cell Cycle of Pancreatic Cancer Cells Through the MAPK/ERK Signaling Pathway.

Background: As a commonly identified cancer in clinics, pancreatic cancer (PC) has poor prognostic outcomes. This work focused on clarifying the association between MIR‐766‐3P expression and PC development and progression, as well as the possible role as a biomarker in PC. Methods: MIR‐766‐3P expression within the human PC cells and samples was measured through miRNA RT‐PCR. The gene levels regulated by MIR‐766‐3P were analyzed through western blot (WB) and qRT‐PCR. To analyze whether MIR‐766‐3P was of certain significance in in vitro and in vivo PC cell proliferation, stemness, and cell cycle progression, the gain/loss‐of‐function assays were performed. Bioinformatics, RNA sequencing (RNA‐seq), and luciferase reporter assay were conducted for exploring regulatory role of MIR‐766‐3P/MAPK1/MAPK/ERK signal axis in PC. Result: In comparison with the normal controls, MIR‐766‐3P expression markedly decreased the tissues and cells of PC. Furthermore, MIR‐766‐3P could remarkably inhibit the proliferation, stemness, cell cycle progression, and development of PC. The analyses using RNA‐seq, and dual‐luciferase examination showed that MIR‐766‐3P could directly target mitogen‐activated protein kinase 1 (MAPK1). According to Gene Ontology (GO) as well as Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, MIR‐766‐3P could affect PC malignant phenotype by MAPK1 and the regulation of the MAPK/ERK‐related pathway. Conclusion: MIR‐766‐3P has a certain impact on PC malignant phenotype through combining with MAPK1 while regulating MAPK/ERK‐related pathway in vitro and in vivo. [ABSTRACT FROM AUTHOR]