GOLPH2, a gene downstream of Ras signaling, promotes the progression of pancreatic ductal adenocarcinoma

Abstract

Various studies have previously demonstrated that Golgi protein-73 (GOLPH2) is overexpressed in tumorigenesis, which has been observed in hepatocellular carcinoma and prostate cancer. However, the expression levels and specific functions of GOLPH2 in the progression of pancreatic cancer remain to be elucidated. The present study aimed to investigate the expression of GOLPH2 in pancreatic ductal adenocarcinoma (PDAC) tissues and examined the effects of GOLPH2 on the growth and migration of pancreatic cancer cells. In the present study, the mRNA levels of GOLPH2 in PDAC cancer tissues were examined using RT-qPCR. The effects of GOLPH2 on the growth and migration of cancer cells were examined using crystal violet and Boyden chamber assays. The study demonstrated that the expression of GOLPH2 mRNA and protein was elevated in PDAC clinical tissues. The growth and motility of the PDAC cells was enhanced following overexpression of GOLPH2, whereas downregulating the expression of GOLPH2 impaired the growth, motility and tumorigenesis. Furthermore, GOLPH2 was observed to interact with protein kinase B (Akt), which subsequently increased the activity of Akt. In addition, GOLPH2 was revealed as a downstream gene of Ras signaling and promoted the transformation of normal pancreatic cells. The results of the present study revealed the important functions of GOLPH2 in PDAC, and suggest that GOLPH2 may act as a promising therapeutic target for the treatment of PDAC in the future.