Abstract
LncRNA down syndrome cell adhesion molecule antisense 1 (DSCAM-AS1) plays an important role in tumor progression, but its function in pancreatic cancer is unknown. DSCAM-AS1 level was evaluated by in situ hybridization (ISH) assay and qRT-PCR. DSCAM-AS1 was knocked down in pancreatic cancer cells, and its impacts on cell proliferation, invasion, and migration were detected. The binding relationship among DSCAM-AS1, miR-136-5p, and pre-B-cell leukemia homeobox 3 (PBX3) was investigated by bioinformatic analysis and luciferase reporter assay. An in vivo animal model was constructed to determine the role of DSCAM-AS1 in tumor growth. Our results showed that DSCAM-AS1 was elevated in tumor tissues of pancreatic cancer patients and cell lines. DSCAM-AS1 knockdown efficiently inhibited PANC-1 cell proliferation, migration, and invasion and suppressed tumor growth. DSCAM-AS1 could promote PBX3 expression by sponging miR-136-5p, and its function in pancreatic cancer was partially mediated by the miR-136-5p/PBX3 axis. Overall, DSCAM-AS1 knockdown inhibits pancreatic cancer progression by modulating the miR-136-5p/PBX3 axis.