DGCR5 is Activated by PAX5 and Promotes Pancreatic Cancer via Targeting miR-3163/TOP2A and Activating Wnt/β-Catenin Pathway

Background: DiGeorge syndrome critical region gene 5 (DGCR5) has been shown to be associated with cancer development. However, the biological role and molecular mechanism of DGCR5 in pancreatic (PC) remains largely unknown. Methods: qRT-PCR fluorescence situ hybridization was performed investigate correlation between expression prognosis clinicopathologic characteristics PC patients. The effects on were studied by gain & loss-of-function experiments vitro vivo. RNA sequencing, bioinformatics analyses, dual-luciferase assays, chromatin immunoprecipitation assay rescue provided insights into underlying competing endogenous (ceRNA) network promoting progression. Results: highly expressed tissues compared adjacent normal its high poor Furthermore, depletion inhibited proliferation, migration invasion increasing apoptosis inducing G0/G1 cell cycle arrest vitro. Moreover, xenograft validated that promotes tumor growth Mechanistically, found act as a ceRNA sponging miR-3163 regulate TOP2A inhibit Wnt/β-catenin pathway. In addition, we downregulation could enhance sensitivity cells gemcitabine, ChIP showed transcription factor PAX5 bind promoter increase transcription. Conclusions: Our study demonstrates is activated progression activating wnt/β-catenin pathway, suggesting may potential diagnostic therapeutic target for PC.