MAP17 as a Mediator of HGF-induced Proliferation and Invasion in Gastric Cancer

Background/Aim: The 17 kDa membrane-associated protein (MAP17) is a non-glycosylated protein localized to the Golgi apparatus and plasma membrane. It is overexpressed in various cancer cells and has been implicated in promoting cancer progression. This study aimed to investigate the role of MAP17 in the proliferation and invasion of gastric cancer cells.

Materials and Methods: To examine the role of MAP17 in carcinoma progression, we performed a series of in vitro and in vivo experiments. In vitro analyses included cell culture experiments, reverse transcription polymerase chain reaction (RT-PCR), complementary DNA (cDNA) microarray, western blot analysis, zymography, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, standard two-chamber invasion assay, and MAP17 knockdown using short hairpin RNA (shRNA). For in vivo analysis, MAP17 enzyme-linked immunosorbent assays (ELISA) were performed on thirty-five blood samples from patients who underwent surgical resection for gastric cancer.

Results: MAP17 expression was up-regulated by HGF in human gastric cancer cells, leading to increased MMP9 expression. Treatment with the PI3K inhibitor LY294002 reduced MMP9 levels. MAP17 knockdown resulted in decreased MMP9 and increased Rac1 expression. Furthermore, MAP17 suppression reduced HGF-induced cell proliferation and invasion while promoting reactive oxygen species (ROS) accumulation. In vivo, a statistically significant decrease in serum MAP17 levels was observed after subtotal or total gastrectomy.

Conclusion: MAP17 plays a crucial role in the proliferation and invasion of gastric cancer cells, suggesting its potential as a biomarker and therapeutic target for gastric cancer.