Long non-coding RNA SUMO1P3 may promote cell proliferation, migration, and invasion of pancreatic cancer via EMT signaling pathway.

Abstract

Long non-coding RNAs (lncRNAs) have been suggested to serve important roles in the development of a number of human cancer types. An increasing amount of data has indicated that the lncRNA small ubiquitin-like modifier 1 (SUMO1) pseudogene 3 (SUMO1P3) has been involved in various types of human cancer. However, the function SUMO1P3 in the development of pancreatic cancer remains unclear. Firstly, reverse transcription-quantitative polymerase chain reaction was performed to determine the expression of SUMO1P3 in pancreatic cancer tissues and cell lines. Then, cell counting kit-8, wound-healing and transwell assays were conducted to explore the effect of SUMO1P3 on pancreatic cancer cell proliferation, migration and invasion. Finally, the EMT-associated proteins were evaluated by western blotting. The results of the present study revealed that SUMO1P3 expression was elevated in pancreatic tissues compared with the corresponding adjacent normal tissues. Additionally, the data indicated that the increased expression of SUMO1P3 is significantly associated with tumor progression and the poor survival of patients with pancreatic cancer. Furthermore, the present study identified that SUMO1P3 knockdown may suppress the proliferation, migration and invasion of pancreatic cancer cells. Additionally, downregulation of SUMO1P3 suppressed the epithelial-mesenchymal transition (EMT) and increased the expression of epithelial cadherin, and decreased the expression of neuronal cadherin, vimentin and β-catenin. Taken together, the results of the present study demonstrated that SUMO1P3 may participate in EMT and pancreatic cancer progression, thus suggesting that it may be a novel diagnostic and therapeutic biological target for pancreatic cancer.