| Objective:Long noncoding RNAs(lnc RNA)participate in regulation of gene expression and biology manipulation and altered lnc RNA expression associated with cancer development and progression.The lnc RNA SCAMP1 expression was aberrant and changed various cancer malignant behaviors.This study assessed SCAMP1 expression in pancreatic ductal adenocarcinoma(PDAC)for association with clinicopathological features and survival of patients and then explored the underlying molecular events.Methods:Bioinformatics analysis technology were used to study the expression level of PDAC in cancer tissues and adjacent normal tissues.The relationship between SCAMP1 expression and survival rate was analyzed.The biological function of SCAMP1 in PDAC was clarified by detecting epithelial-mesenchymal transition markers and performing CCK-8,colony formation,transwell invasion assays and nude mouse tumor cell xenograft assay.After that,the mechanism of SCAMP1 in promoting PDAC progression was further studied by conducting subcellular fractionation assay,luciferase reporter gene assay,RNA immunoprecipitation(RIP)assay and q RT-PCR experiments.Results:The data showed that SCAMP1 expression was significantly upregulated in PDAC tissues,which was associated with poor survival of patients.Knockdown of SCAMP1 expression reduced tumor cell proliferation,invasion,and epithelial?mesenchymal transition(EMT)in vitro and suppressed tumor cell xenograft growth in nude mice.At gene levels,SCAMP1 was able to target miR-106a-5p to in turn upregulate acylglycerol kinase(AGK)expression and promote PDAC malignant behaviors in vitro.Conclusion:This study demonstrates that SCAMP1 plays a tumor-promoting role in PDAC by targeting the miR-106a-5p/AGK signaling axis.Therefore,this study suggests that targeting the SCAMP1/miR-106a-5p/AGK signaling axis may become a new strategy for pancreatic cancer treatment in the future. |
