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This Article Full Text Full Text (PDF) All Versions of this Article: gut.2005.078113v1 55/6/797    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this link to a friend Similar articles in this journal Similar articles in PubMed Add article to my folders Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by He, X-X Articles by Xia, H H-X Search for Related Content PubMed PubMed Citation Articles by He, X-X Articles by Xia, H H-X

Increased epithelial and serum expression of macrophage migration inhibitory factor (MIF) in gastric cancer: potential role of MIF in gastric carcinogenesis

¹ Department of Gastroenterology, The Second Affiliated Hospital of Guangzhou Medical College, Guangzhou, Guangdong, China
² Department of Epidemiology, Roswell Park Cancer Institute, Buffalo, New York, USA
³ Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China

Correspondence to:
Correspondence to:
Dr H H-X Xia
Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China; hhxxia{at}hku.hk

Aims: Macrophage migration inhibitory factor (MIF) is implicated in tumorigenesis. This study was conducted to determine whether MIF expression is associated with gastric pathology and whether MIF expression is increased in malignant gastric cells in vitro.

Materials and methods: Patients with a normal gastric mucosa, Helicobacter pylori infected gastritis, intestinal metaplasia, and gastric adenocarcinoma were included. Immunohistochemistry and enzyme linked immunosorbent assay (ELISA) were used to determine MIF expression in gastric epithelial cells and MIF levels in serum, respectively. Five gastric cancer cell lines (AGS, MKN-45, MKN-28, MGC-803, and SGC-7901) and one non-malignant gastric cell line (GES-1) were cultured for 24 hours. MIF protein in the supernatant and MIF mRNA in cultured cells were measured by ELISA and reverse transcription-polymerase chain reaction, respectively.

Results: The percentage of MIF expressing epithelial cells was low in normal mucosa (12%) but substantially higher in gastritis (52%), intestinal metaplasia (66%), and gastric cancer (96%) (p<0.001, ANOVA). Serum MIF levels were low in patients with a normal mucosa (576 (82) pg/ml) but higher in patients with gastritis (2100 (349) pg/ml), intestinal metaplasia (4498 (253) pg/ml), and gastric cancer (9737 (1249) pg/ml) (p<0.001, ANOVA). There was a correlation between epithelial MIF expression and serum MIF levels (r = 0.776, p<0.001). In vitro, expression of MIF protein and mRNA was increased in malignant cells compared with non-malignant cells.

Conclusions: Epithelial and serum MIF expression was progressively increased in H pylori induced gastritis, intestinal metaplasia, and gastric cancer, suggesting that MIF is involved in gastric carcinogenesis and may be a valuable biomarker for the early detection of gastric cancer.

Abbreviations: MIF, macrophage migration inhibitory factor; ELISA, enzyme linked immunosorbent assay; RT-PCR, reverse transcription-polymerase chain reaction; LI, labelling index

Keywords: macrophage migration inhibitory factor; Helicobacter pylori infection; intestinal metaplasia; gastric cancer