HMGN5 promotes proliferation and invasion via the activation of Wnt/β-catenin signaling pathway in pancreatic ductal adenocarcinoma.

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive carcinoma with a poor prognosis. A recent study has demonstrated that high mobility group nucleosome binding domain 5 (HMGN5) was involved in tumorigenesis and progression of multiple types of human cancers. However, the role of HMGN5 in PDAC is unknown. The objective of the present study was to analyze the function and novel mechanism of HMGN5 involved in PDAC cell progression. It was firstly revealed that the expression of HMGN5 was significantly upregulated in PDAC cell lines and tissues, when compared with that in normal pancreatic duct epithelial cells and adjacent normal pancreatic tissues. In vitro assay revealed that HMGN5 silencing impaired PDAC cell viability, proliferation, migration and invasion. Similarly, tumor growth rate was also decreased in vivo following HMGN5 silencing. Furthermore, it was demonstrated that HMGN5 silencing significantly inhibited epithelial-mesenchymal transition in vitro. Notably, HMGN5-medicated Wnt/β-catenin signaling pathway activation was observed to be one of the critical signal transduction pathways that associates HMGN5 with EMT activation. Collectively, the results indicated the important role of HMGN5 in PDAC cell proliferation and metastasis, and provide a promising target against the transcriptional program of PDAC.