TRIM37 promoted the growth and migration of the pancreatic cancer cells.

Abstract

Increasing evidence indicated that tripartite motif containing 37 (TRIM37) was involved in the tumorigenesis of several cancer types. However, its expression pattern and biological functions in pancreatic ductal adenocarcinoma (PDAC) remained unknown. In this study, real-time PCR, Western blot and immunohistochemistry was performed to examine the expression of TRIM37 in the pancreatic cancerous tissues. Colony formation assay and cell migration assay were performed to study the functions of TRIM37 in pancreatic cancer cells. Dual-luciferase assay was performed to study the regulation of TRIM37 on beta-catenin/TCF signaling. It was found that the expression level of TRIM37 was significantly higher in pancreatic cancerous tissues compared with the adjacent normal tissues. Function analysis indicated that overexpression of TRIM37 promoted the growth and migration of the pancreatic cancer cells, while knocking down the expression of TRIM37 inhibited the growth and migration of the pancreatic cancer cells. The molecular mechanism study suggested that TRIM37 interacted with beta-catenin and activated the transcriptional activity of beta-catenin/TCF complex as well as the expression of its downstream target genes. Taken together, our study showed the oncogenic roles of TRIM37 in pancreatic cancer, and TRIM37 might be a promising target for pancreatic cancer treatment.