The Lncrna-TUG1/EZH2 Axis Promotes Pancreatic Cancer Cell Proliferation, Migration and EMT Phenotype Formation Through Sponging Mir-382.

摘要: Background/Aims: Pancreatic carcinoma (PC) is the one of most common and malignant cancers worldwide. LncRNA taurine upregulated gene 1 (TUG1) was initially identified as a transcript by taurine, abnormal expression TUG1 has been reported in many cancers. However, biological role molecular mechanism PC still needs further investigation. Methods: Quantitative real-time PCR (qRT-PCR) performed to measure cell lines tissues. MTT colony formation assays were used effect on proliferation. A wound healing assay, transwell assay western blot employed determine migration epithelial mesenchymal transition (EMT) phenotype. RNA-binding protein immunoprecipitation (RIP) biotin-avidin pulldown system confirm interaction between miR-328 TUG1. array analysis using clinical samples RT-qPCR suggested that enhancer zeste homolog 2 (EZH2) target miR-382 PC. Results: In this study, we overexpressed tissues lines, high predicted poor prognosis. Further experiments revealed promoted proliferation, contributed EMT formation, whereas silenced led opposing results. Additionally, luciferase reporter assays, an RIP RNA-pulldown demonstrated could competitively sponge thereby regulate EZH2. Conclusion: Collectively, these findings functions oncogenic lncRNA promotes tumor progression, at least partially, functioning endogenous ‘sponge’ competing for binding miRNA