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

TitleIncreased epithelial and serum expression of macrophage migration inhibitory factor (MIF) in gastric cancer: potential role of MIF in gastric carcinogenesis
Authors
Issue Date2006
PublisherB M J Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/
Citation
Gut, 2006, v. 55 n. 6, p. 797-802 How to Cite?
AbstractAIMS: 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.
Persistent Identifierhttp://hdl.handle.net/10722/45004
ISSN
2023 Impact Factor: 23.0
2023 SCImago Journal Rankings: 8.052
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHe, XXen_HK
dc.contributor.authorYang, Jen_HK
dc.contributor.authorDing, YWen_HK
dc.contributor.authorLiu, Wen_HK
dc.contributor.authorShen, QYen_HK
dc.contributor.authorXia, HHXen_HK
dc.date.accessioned2007-10-30T06:15:25Z-
dc.date.available2007-10-30T06:15:25Z-
dc.date.issued2006en_HK
dc.identifier.citationGut, 2006, v. 55 n. 6, p. 797-802en_HK
dc.identifier.issn0017-5749en_HK
dc.identifier.urihttp://hdl.handle.net/10722/45004-
dc.description.abstractAIMS: 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.en_HK
dc.format.extent890072 bytes-
dc.format.extent1826 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypetext/plain-
dc.languageengen_HK
dc.publisherB M J Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/en_HK
dc.rightsGut. Copyright © B M J Publishing Group.en_HK
dc.subject.meshAdenocarcinoma - metabolismen_HK
dc.subject.meshMacrophage Migration-Inhibitory Factors/blood - metabolismen_HK
dc.subject.meshPrecancerous Conditions - metabolismen_HK
dc.subject.meshStomach Neoplasms - metabolismen_HK
dc.subject.meshTumor Markers, Biological - blood - metabolismen_HK
dc.titleIncreased epithelial and serum expression of macrophage migration inhibitory factor (MIF) in gastric cancer: potential role of MIF in gastric carcinogenesisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0017-5749&volume=55&issue=6&spage=797&epage=802&date=2006&atitle=Increased+epithelial+and+serum+expression+of+macrophage+migration+inhibitory+factor+(MIF)+in+gastric+cancer:+potential+role+of+MIF+in+gastric+carcinogenesisen_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1136/gut.2005.078113en_HK
dc.identifier.pmid16488898-
dc.identifier.pmcidPMC1856238-
dc.identifier.scopuseid_2-s2.0-33646820643-
dc.identifier.isiWOS:000237471400014-
dc.identifier.issnl0017-5749-

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