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Bridging Inflammation and Oncology: The Role and Therapeutic Potential of Macrophage Migration Inhibitory Factor in
Mohammed Ali Selo1,2, Oliviero L Gobbo3,4, Ismael Obaidi1,5
1School of Medicine, Trinity Biomedical Sciences Institute (TBSI), Trinity College Dublin, D02 R590 Dublin, Ireland.
Abstract:
Lung cancer is the leading cause of cancer-related mortality worldwide, accounting for more deaths than any other malignancy. Despite advances in treatment, it remains highly lethal, with 5-year survival rates showing minimal improvement over the past several decades, highlighting a critical unmet clinical need. Macrophage Migration Inhibitory Factor (MIF) is a multifunctional cytokine that contributes to inflammation and cancer, promoting tumor growth, progression, and metastasis through modulation of the tumor microenvironment, stimulation of angiogenesis, and regulation of immune responses. Polymorphisms in the promoter region of MIF, such as high-expression CATT repeats, influence MIF expression and susceptibility to a range of inflammatory, autoimmune, and malignant disorders, yet their role in lung cancer remains largely unexplored. Therapeutic strategies targeting MIF, including small-molecule inhibitors, antibodies, and peptide-based agents, have shown promise in preclinical models, although their clinical translation is still limited. This review discusses the dual role of MIF in inflammation and oncology, summarizes current therapeutic developments, and emphasizes the potential of MIF-targeted interventions in lung cancer. It discusses the significance of genetic predisposition, particularly high-expression MIF alleles, in guiding personalized treatment strategies for lung cancer and identifying patients who may derive benefit from MIF inhibition.
Insights
Macrophage Migration Inhibitory Factor (MIF) drives lung cancer progression. Targeting MIF, especially in patients with high-expression alleles, offers a promising personalized therapeutic strategy for this lethal disease.
Area of Science:
- Oncology
- Immunology
- Genetics
Background:
- Lung cancer is a leading cause of cancer mortality globally, with limited survival improvements despite treatment advances.
- Macrophage Migration Inhibitory Factor (MIF) is a key cytokine implicated in inflammation and cancer, promoting tumor growth, angiogenesis, and immune evasion.
- Genetic variations, like high-expression MIF CATT repeats, affect susceptibility to diseases, but their role in lung cancer is understudied.
Purpose of the Study:
- To review the dual role of MIF in inflammation and lung cancer.
- To summarize current therapeutic strategies targeting MIF.
- To highlight the potential of MIF-targeted therapies and genetic predisposition in personalized lung cancer treatment.
Main Methods:
- Literature review of MIF's role in inflammation and oncology.
- Analysis of preclinical data for MIF-targeted therapies.
- Discussion of genetic polymorphisms and their impact on MIF expression and lung cancer.
Main Results:
- MIF promotes lung cancer progression by modulating the tumor microenvironment, angiogenesis, and immune responses.
- Preclinical studies show promise for MIF inhibitors, antibodies, and peptide-based agents.
- High-expression MIF alleles may identify patients who could benefit from MIF inhibition.
Conclusions:
- MIF plays a significant role in lung cancer development and progression.
- Targeting MIF presents a potential therapeutic avenue for lung cancer.
- Genetic screening for MIF polymorphisms could enable personalized treatment strategies for lung cancer patients.
