Lin28B/Let-7 Pathway Involves In The Induction Of Gemcitabine Drug Resistance Of Pancreatic Cancer

Objective: To confirm the molecular mechanism and the relationship between Lin28B/let-7 pathway with pancreatic cancer chemotherapy resistance by targeting.Furthermore,to investigate the effect of changing Lin28B/let-7 pathway on gemcitabine resistance of human pancreatic cancer cells.Methods: Pancreatic Aspc-1 cells were divided into overexpression group,silencing group and control.By transient transfection technology,Overexpression: pCMV6-Lin28 B plasmids and pCMV6.Silencing:pGFP-shLin28 B and pGFP were respectively transfected intopancreatic AsPC-1 cells.Western blotting analysis Lin28 B protein,realtime fluorescence quantitative PCR identified Lin28 B mRNA and let-7 family microRNAs.Finally,the transfection of AsPC-1 Cells were treated with gemcitabine at the indicated concentrations.After 72 h of incubation,cell viability was measured by MTS assay to reflect the drug resistance.Results: pCMV6-Lin28 B plasmid enables to Lin28 B protein effective overexpression,in contrast pGFP-shLin28 B plasmid make Lin28 B protein decreased.Meanwhile Let-7microRNA expression level there was a significant difference.Introduction of Lin28Bhigh/let-7low increased the gemcitabine resistance,While Lin28Blow/let-7high reduced it.Conclusion: Lin28 B targeting let-7 family microRNA may be involved in the induction of gemcitabine drug resistance of pancreatic cancer cells.