LINC00857 Facilitates Proliferation and Malignancy of Pancreatic Ductal Adenocarcinoma Cells via AKT/beta-Catenin Signaling

Background: LINC00857 plays an oncogenic role in several cancer types. The aim of this study is to evaluate the role of LINC00857 in pancreatic ductal adenocarcinoma (PDAC) and understand its mechanism. Methods: Firstly, LINC00857 expression in PDAC was predicted using TCGA (The Cancer Genome Atlas) database followed by its determination in clinical PDAC tissues by RT-PCR (reverse transcription-polymerase chain reaction) analysis. Then, MIA PaCa-2 and PANC-1 pancreatic cancer cells were transfected with siRNAs of LINC00857, followed by CCK-8 (Cell Counting Kit-8), cell colony formation, cell apoptosis, cell scratch, and trans-well invasion assay. Besides, p-AKT(phosphorylated protein kinase B), ss-catenin, Bax, and cleaved caspase3 levels were detected by western blot analysis. Finally, subcutaneous nude mouse models were created with PANC-1 cells transfected with si-LINC00857 or si-NC. Results: LINC00857 was overexpressed in PDAC and related to poor prognosis. This was validated in clinical PDAC tissues. When LINC00857 was silenced the proliferation, migration, and invasion was impaired but apoptosis of PDAC cells was induced. In addition, western blot analysis showed a correlation between LINC00857 and AKT/ss-catenin. Si-LINC00857 reduced the protein level of p-AKT and ss-catenin. Tumor volume and tumor weight declined in si-LINC00857 transfection group, compared to that in si-NC transfection group. Conclusions: LINC00857 knockdown suppressed proliferation, migration and invasion of PDAC cells through AKT/ss-catenin signaling in part.