Human GLTP inhibits growth of pancreatic cells via regulation of PI3K/Akt signaling

Pancreatic cancer (PC) is a very heterogeneous and often fatal disease, primarily due to the diversity of genetic mutations present. Additionally, it is often highly aggressive and exhibits drug resistance. The availability of biomarkers with suitable accuracy for early screening of PC is limited. Therefore, more effective early diagnostic markers and potential therapeutic targets for PC are required. The human glycolipid transfer protein (GLTP) is a member of the GLTP protein superfamily, and is involved in cell cycle progression and necroptosis physiologically, and in hepatitis C, colorectal cancer, and other disease processes pathophysiologically. However, the role of GLTP in PC remains to be determined. In the present study, the expression of GLTP in PC tissues and its relationship with clinicopathological features of PC patients was assessed for the first time. The results showed that GLTP expression was downregulated in PC tissues and was associated with the individual cancer stages, tumor grades, and age. Next, the effect of GLTP on the proliferation, migration, invasion, and oncogenicity of PC cells was assessed. In addition, the possible mechanism of GLTP action on PC cells at the molecular level was assessed. It was found that GLTP inhibited the proliferation, migration, and invasion of PC cells by downregulating the PI3K/Akt signaling. The PI3K/Akt signaling may be downregulated by GLTP in PC, making it a potential therapeutic target.