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Onco Targets Ther. 2017 Oct 24;10:5151-5163. doi: 10.2147/OTT.S148681. eCollection 2017.

Overexpression of MPC1 inhibits the proliferation, migration, invasion, and stem cell-like properties of gastric cancer cells.

Author information

1
Department of Gastrointestinal Surgery, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu.
2
Nutritional Center, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu.
3
Department of Thoracic Oncology, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.

Abstract

Invasion and metastasis are major malignant characteristics of human gastric cancer (GC), but the molecular mechanisms underlying the invasion and metastasis of GC cells remain elusive. MPC1, a key factor that controls pyruvate transportation through the inner mitochondrial membrane, was reported to be downregulated and correlated with poor prognosis in several cancers. However, the effects of MPC1 on human GC have not been illustrated. In this study, we investigated the potential role of MPC1 in the proliferation, migration, invasion, and stem cell-like properties of human GC cells and evaluated its prognostic significance for patients with GC. We found that MPC1 protein and mRNA levels were significantly decreased in GC tissues and cell lines. Low MPC1 expression was associated with tumor T stage, N stage, and advanced tumor node metastasis stage. Decreased MPC1 expression was an independent prognostic marker and correlated with poor overall survival of patients with GC. Furthermore, overexpression of MPC1 inhibited the proliferation, migration, invasion, and stem cell-like properties of GC cells. These findings suggest that MPC1 may be a novel prognostic marker and a potential therapeutic target in human GC.

KEYWORDS:

MPC1; gastric cancer; invasion; migration; proliferation

Conflict of interest statement

Disclosure The authors report no conflicts of interest in this work.

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