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Updated: Jan 29, 2026

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance
Published on: March 7, 2025
Correlation between macrophage migration inhibitory factor and autophagy in Helicobacter pylori-associated gastric
Kichul Yoon1, Nayoung Kim1,2, Youngmi Park3
1Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, South Korea.
Abstract:
The role of macrophage migration inhibitory factor (MIF) and autophagy in gastric cancer is not clear. We determined H. pylori infection status of the subjects and investigated the expression of MIF and autophagy markers (Atg5, LC3A and LC3B) in human gastric tissue at baseline. Then H. pylori eradication was done for H. pylori positive patients and MIF and Atg5 levels were investigated on each follow-up for both H. pylori-eradicated and H. pylori negative patients. Baseline tissue mRNA expression of MIF, Atg5, LC3A and LC3B was measured by real-time PCR in 453 patients (control 165, gastric dysplasia 82, and gastric cancer 206). Three hundred three patients (66.9%) had H. pylori infection at the time of enrollment. Only within H. pylori-positive group, MIF level was significantly elevated in patients with cancer than in control or dysplasia groups (P<0.05). LC3A and LC3B levels also showed significant differences within H. pylori-positive subgroups. H. pylori-positive dysplasia subgroup showed significantly lower (LC3A) (P<0.05) and higher (LC3B) mRNA levels (P<0.05) than in other subgroups. On follow-up, within H. pylori-eradicated group, Atg5 expression increased sequentially from control to dysplasia and cancer subgroups. Multiple linear regression showed autophagy markers (LC3A, LC3B, and Atg5) directly predicted MIF level (adjusted R2 = 0.492, P<0.001). Serial follow-up showed longitudinal increase in Atg5 level in general, with constantly higher levels in H. pylori-eradicated group than in -negative group. Intestinal metaplasia (IM) group initially showed higher Atg5 expression than the IM-negative group. However, it was reversed between the groups eventually because of the lower rate of increase in IM group. These results suggest a role of MIF and autophagy markers and their interaction in H. pylori-associated gastric carcinogenesis.
Insights
Macrophage migration inhibitory factor (MIF) and autophagy markers play a role in H. pylori-associated gastric cancer. Their interaction suggests a link to gastric carcinogenesis.
Area of Science:
- Gastroenterology
- Oncology
- Molecular Biology
Background:
- The roles of macrophage migration inhibitory factor (MIF) and autophagy in gastric cancer remain unclear.
- Helicobacter pylori (H. pylori) infection is a known risk factor for gastric cancer.
- Autophagy markers include Atg5, LC3A, and LC3B.
Purpose of the Study:
- To investigate the expression of MIF and autophagy markers in relation to H. pylori infection and gastric carcinogenesis.
- To explore the interaction between MIF and autophagy markers in H. pylori-associated gastric cancer.
Main Methods:
- Real-time PCR was used to measure mRNA expression of MIF, Atg5, LC3A, and LC3B in 453 patients (control, gastric dysplasia, gastric cancer).
- H. pylori infection status was determined, and eradication therapy was performed for positive patients.
- MIF and Atg5 levels were monitored during follow-up in H. pylori-eradicated and H. pylori-negative groups.
- Multiple linear regression analysis was employed to assess the predictive value of autophagy markers on MIF levels.
Main Results:
- In H. pylori-positive patients, MIF levels were significantly elevated in the cancer group compared to control or dysplasia groups.
- Autophagy markers LC3A and LC3B showed significant differences within H. pylori-positive subgroups.
- Atg5 expression increased sequentially from control to cancer subgroups in the H. pylori-eradicated group.
- Autophagy markers (LC3A, LC3B, Atg5) were direct predictors of MIF levels (adjusted R2 = 0.492, P<0.001).
- H. pylori-eradicated patients consistently showed higher Atg5 levels than H. pylori-negative patients during follow-up.
Conclusions:
- MIF and autophagy markers, particularly in the context of H. pylori infection, are implicated in gastric carcinogenesis.
- The interaction between MIF and autophagy markers appears to be a significant factor in the development of gastric cancer.
- Further research into these molecular pathways could lead to novel diagnostic or therapeutic strategies for H. pylori-associated gastric cancer.
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