ABSTRACT
Ubiquitin-like with PHD and ring finger domains 1 (UHRF1) has been reported as a marker for the differential diagnosis of pancreatic cancer and chronic pancreatitis. However, the expression pattern and biological functions of UHRF1 in the progression of pancreatic cancer are not fully understood. In this study, it was found that the expression of UHRF1 was significantly up-regulated in pancreatic cancer samples compared to their adjacent normal tissues. Meanwhile, the expression of UHRF1 was inversely correlated with the survival of pancreatic cancer patients. Moreover, in the biological function studies, UHRF1 was shown to promote the growth, migration, and metastasis of pancreatic cancer cells in vitro and in vivo. Mechanistically, the expression of UHRF1 was induced by oncogenic Ras in both pancreatic cancer mouse model and cultured cells. Taken together, our study demonstrated that UHRF1 played an oncogenic role in the progression of pancreatic cancer, and UHRF1 might be a promising target for the treatment of pancreatic cancer.
Subject(s)
CCAAT-Enhancer-Binding Proteins/biosynthesis , Cell Proliferation/genetics , Genes, ras/genetics , Pancreatic Neoplasms/genetics , Animals , Cell Line, Tumor , Cell Movement/genetics , Gene Expression Regulation, Neoplastic , Humans , Mice , Neoplasm Metastasis , Pancreatic Neoplasms/pathology , Ubiquitin-Protein Ligases , Xenograft Model Antitumor AssaysABSTRACT
NOV, a member of the CCN (Cyr61, CTGF and NOV) family, is involved in diverse biological processes, such as cell adhesion, proliferation and angiogenesis. However, its function in pancreatic cancer remains poorly understood. Here, we found that the expression of NOV was up-regulated in pancreatic cancer tissues. Moreover, over-expression of NOV in pancreatic cancer cells promoted cell proliferation and migration, while knock down the expression of NOV impaired the tumorigenecity of pancreatic cancer cells in vitro and in vivo. Mechanistically, NOV induced epithelial-mesenchymal transition (EMT) and regulated the expression of multiple EMT marker. Taken together, our study suggested the important role of NOV in pancreatic cancer and NOV might be an important therapeutic target.
