Abstract
Our study investigated competitive endogenous RNAs (ceRNAs) in pancreatic cancer by sequencing clinical samples, aiming to identify diagnostic markers and therapeutic targets. We conducted transcriptome sequencing on pancreatic ductal adenocarcinoma (PDAC) tumor tissues and normal tissues from five cases. MiR-199a-5p expression was measured in ten cancer-normal tissue pairs using quantitative PCR (qPCR). In vitro, cell lines were transfected with miR-199a-5p mimic, inhibitor, and controls. MiR-199a-5p antagomir was locally injected in a mouse xenograft model. Our findings revealed a novel regulatory pathway involving VASH1-AS1/miR-199a-5p/PDCD4 in PDAC. Dual-luciferase reporter assays confirmed direct binding between VASH1-AS1 and miR-199a-5p. Inhibiting miR-199a-5p led to significant in vivo tumor growth inhibition. We validated PDCD4’s function in PDAC formation using overexpression vectors and PDCD4-targeting siRNA. Our research suggests that reduced VASH1-AS1 expression in PDAC up-regulates miR-199a-5p, inhibiting PDCD4 and promoting PDAC formation. The study highlights the pivotal role of miR-199a-5p, VASH1-AS1, and PDCD4 in pancreatic cancer’s occurrence and progression In vitro and in vivo.
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