Abstract
BACKGROUND: Long intergenic nonprotein coding RNA 1503 (LINC01503) was reportedly oncogenic in several malignancies, whereas whether it contributed to pancreatic cancer tumorigenesis and progression requires to be verified. METHODS: The expression pattern of LINC01503 was monitored via qRT-PCR assay in normal cells and cancerous pancreatic cancer cells. The introduction of silencing LINC01503 was to verify the relation between LINC01503 expression and cell growth. Then, the targeting relationship of LINC01503 to miR-1321 was confirmed by bioinformatics predication and luciferase reporter assay. In addition, luciferase reporter assays evaluated the binding of miR-1321 to the 3'-untranslated region of KLK4. Overexpressing KLK4 and inhibiting LINC01503 was introduced in tumor cells to investigate the corresponding impacts on pancreatic cancer cell proliferation and migration. RESULTS: LINC01503 and KLK4 were highly abundant in pancreatic cancer cells. Mechanistically, miR-1321 bound to LINC01503 and KLK4. Downregulating LINC01503 promoted the availability of miR-1321 in pancreatic cancer cells and thus repressed KLK4 expression. KLK4 overexpression abolished the impediment of LINC01503 depletion on cell proliferation and migration. CONCLUSION: Oncogenic function of LINC01503 was dependent on KLK4 upregulation by sponging miR-1321. Revealing the tumor-promoting property of LINC01503 in pancreatic cancer may confer new biomarkers for this malignancy.