The objective of the present study was to clarify the expression characteristics of long non-coding RNA (lncRNA) FGD5 antisense RNA 1 (FGD5-AS1) in pancreatic cancer, as well as its biological function and underlying mechanism. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was utilized for the detection of FGD5-AS1 and microRNA (miR)-577 expression levels in pancreatic cancer tissues. Transfection was performed to upregulate or downregulate FGD5-AS1 in pancreatic cancer cell lines. MTT and Transwell assays were then utilized to detect the proliferation, migration and invasion of cancer cells, respectively. Subsequently, dual-luciferase reporter gene assay, RNA immunoprecipitation assay, RNA pull-down assay, RT-qPCR, western blotting, and Pearson's correlation analysis were employed to confirm the regulatory relationships among FGD5-AS1, miR-577, low-density lipoprotein receptor-related protein 6 (LRP6) and beta-catenin. Western blotting was employed to determine the expression levels of Axin2, cyclin Dl and c-Myc. The expression level of FGD5-AS1 was upregulated in pancreatic cancer tissues and cell lines. FGD5-AS1 knock-down inhibited pancreatic cancer cell proliferation, migration and invasion. By contrast, miR-577 was significantly inhibited in pancreatic cancer cells and tissues; its downregulation promoted pancreatic cancer cell proliferation, migration and invasion, and reversed the effects of FGD5-AS1 knockdown on pancreatic cancer cells. In addition, it was revealed that miR-577 was a target of FGD5-AS1, and FGD5-AS1 could modulate the expression levels of LRP6, beta-catenin, Axin2, cyclin D1 and c-Myc via suppressing miR-577. In conclusion, in pancreatic cancer, highly expressed FGD5-AS1 activated the Wnt/beta-catenin signaling and promoted cancer cell proliferation, migration and invasion via suppression of miR-577. the Wnt/beta-catenin signaling and promoted cancer cell proliferation, migration and invasion via suppression of miR-577.