Linc-RoR Promotes Epithelial–mesenchymal Transition Via The Hippo Pathway In Pancreatic Cancer Cells

Pancreatic cancer is one of the most common cancers in the world.It is a fatal malignant disease with a median survival of 3-6 months and a 5-year survival rate of less than 5%.Although there are good surgical techniques and adjuvant drugs,the early diagnosis of pancreatic cancer is extremely difficult,the operative mortality is high,and the therapeutic effect of radiotherapy and chemotherapy on pancreatic cancer is poor.Therefore,the prognosis of pancreatic cancer is extremely poor.Therefore,further understanding of the core molecular mechanisms of pancreatic tumorigenesis and exploring new therapeutic targets are critical to improving survival in these patients.Long non-coding RNA(lncRNA)consists of more than 200 nucleotides,which have important gene regulation in normal cells and cancer cells,including genomic imprinting,epigenetic regulation,alternative splicing,cell differentiation and carcinogenesis.Linc-RoR,a classical long non-coding RNA,reprograms differentiated cells into induced pluripotent stem cells(iPSCs)and plays an important role in the progression of many tumors.Objective: To detect the expression of Linc-RoR in pancreatic cancer cells,to clarify the effect of Linc-RoR on the biological behavior of pancreatic cancer cells,and to explore its underlying molecular mechanism,which can be applied to pancreatic cancer by Linc-RoR.Molecular targeted therapy provides a solid theoretical basis.Methods: 1.Real-time PCR was used to analyze the relative expression of Linc-RoR mRNA in pancreatic cancer cells BxPC-3,SW1990 and PaTu8988;2.Transfection of pCDH-RoR plasmid in BxPC-3 and SW1990,in SW1990 and PaTu8988 The sh-RoR plasmid was transfected to verify the efficiency of the plasmid.3.The ability of Linc-RoR to regulate the proliferation and clonal formation of pancreatic cancer cells was analyzed by CCK-8 assay and plate cloning assay.4.Scratch test and Transwell assay were used to analyze Linc.-RoR regulates the migration and invasion ability of pancreatic cancer cells;5.Western blot to verify the relationship between Linc-RoR and protein expression in EMT process of pancreatic cancer cells,and analyze the protein matrix involved in invasion and invasion by Linc-RoR by Western blot Expression of metalloproteinase 2(MMP2)and matrix metalloproteinase 9(MMP9);6.Western blot analysis of the mechanism of Linc-RoR regulation of epithelial-mesenchymal transition in pancreatic cancer cells.Results: 1.Linc-RoR was differentially expressed in three pancreatic cancer cells.The expression of Linc-RoR was highest in PaTu8988 and lowest in BxPC-3.2,up-regulation of Linc-RoR,can promote the proliferation of pancreatic cancer cells and the ability to clone;the down-regulation of Linc-RoR can inhibit the proliferation of pancreatic cancer cells and the ability to clone.3.Up-regulation of Linc-RoR can promote the migration and invasion of pancreatic cancer cells;down-regulation of Linc-RoR can inhibit the migration and invasion of pancreatic cancer cells.4.After up-regulating Linc-RoR,the expression levels of MMP2 and MMP9 increased;after down-regulating Linc-RoR,the expression levels of MMP2 and MMP9 decreased.After up-regulating Linc-RoR,the expression of N-cadherin,vimentin and Snail protein was increased and the expression of E-cadherin protein was decreased.Conversely,after down-regulating Linc-RoR,the expression of N-cadherin,vimentin and Snail protein decreased and E-cadherin protein expression decreased.Raise.6.After up-regulating Linc-RoR,the expression of YAP and MOB1 protein was increased in pancreatic cancer cells,and the expressions of p-YAP,p-MOB1,p-LATS1,LATS1,MST1 and MST2 were decreased.After down-regulating Linc-RoR,the expression of YAP and MOB1 protein was decreased in pancreatic cancer cells,and the expression of p-YAP,p-MOB1,p-LATS1,LATS1,MST1 and MST2 proteins was increased.Conclusion: 1.Linc-RoR has a biological role in promoting the proliferation,migration and invasion of pancreatic cancer cells.2.Linc-RoR promotes epithelial-mesenchymal transition of pancreatic cancer cells by regulating the Hippo signaling pathway.