Role of macrophage migration inhibitory factor in head and neck cancer and novel therapeutic targets: A systematic review

Head & Neck ◽  
2017 ◽  
Vol 39 (12) ◽  
pp. 2573-2584 ◽  
Author(s):  
Jérôme R. Lechien ◽  
Amir Nassri ◽  
Nadege Kindt ◽  
David N. Brown ◽  
Fabrice Journe ◽  
...  
Keyword(s):  
Systematic Review ◽  
Head And Neck Cancer ◽  
Head And Neck ◽  
Neck Cancer ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Novel Therapeutic

Macrophage Migration Inhibitory Factor Modulated Proliferation, Cell Cycle, and Apoptotic Activity in Head and Neck Cancer Cell Lines

2019 ◽  
Author(s):  
Kusumawadee Utispan ◽  
Sittichai Koontongkaew
Keyword(s):  
Cell Cycle ◽  
Head And Neck ◽  
Cell Lines ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Cell Cycle Progression ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Hnscc Cell

Macrophage migration inhibitory factor (MIF) is a multifunctional cytokine that contributes to the progression of several cancers. MIF overexpression has been reported in head and neck squamous cell carcinoma (HNSCC) patients. However, the exact role of MIF in HNSCC is not fully understood. Our aim was to evaluate the amount of secreted MIF and the role of MIF in the proliferation, cell cycle, and apoptosis in HNSCC cell lines. The MIF levels in conditioned media from human primary (HN18 and HN30) and metastatic (HN17 and HN31) HNSCC cell lines were evaluated using ELISA. The HNSCC cell lines were treated with recombinant MIF and its effect on proliferation, cell cycle, and apoptotic status was determined by MTT and flow cytometry, respectively. The HNSCC-secreted MIF concentration ranged from 49.33‒860 pg/ml. Exogenous MIF (25 ng/ml) significantly increased HN18, HN30, and HN31 cell proliferation. Moreover, MIF induced cell cycle progression and inhibited apoptosis in these cells. However, MIF did not affect growth or apoptosis in HN17 cell. In conclusion, the HNSCC cell lines were evaluated secrete MIF. Exogenous MIF promotes various effects on proliferation, cell cycle, and apoptosis in HNSCC cells.

scholarly journals Role of Macrophage Migration Inhibitory Factor in the Regulatory T Cell Response of Tumor-Bearing Mice

2012 ◽  
Vol 189 (8) ◽  
pp. 3905-3913 ◽  
Author(s):  
Susanna Choi ◽  
Hang-Rae Kim ◽  
Lin Leng ◽  
Insoo Kang ◽  
William L. Jorgensen ◽  
...  
Keyword(s):  
T Cell ◽  
Migration Inhibitory Factor ◽  
Regulatory T Cell ◽  
Cell Response ◽  
Macrophage Migration Inhibitory Factor ◽  
T Cell Response ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Tumor Bearing

scholarly journals The role of human macrophage migration inhibitory factor in promoting angiogenesis

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
XiYong Yu ◽  
ZhiXin Shan ◽  
QiuXiong Lin ◽  
ShiXia Cai ◽  
Min Yang ◽  
...  
Keyword(s):  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Human Macrophage ◽  
Macrophage Migration

Role of macrophage migration inhibitory factor in bleomycin-induced lung injury and fibrosis in mice

2002 ◽  
Vol 283 (1) ◽  
pp. L156-L162 ◽  
Author(s):  
Yoshinori Tanino ◽  
Hironi Makita ◽  
Kenji Miyamoto ◽  
Tomoko Betsuyaku ◽  
Yoshinori Ohtsuka ◽  
...  
Keyword(s):  
Lung Injury ◽  
Migration Inhibitory Factor ◽  
Lung Fibrosis ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Lung Injury Score ◽  
Macrophage Migration ◽  
Acute Lung Inflammation ◽  
Intratracheal Administration

Macrophage migration inhibitory factor (MIF) is a unique cytokine that reportedly overrides the anti-inflammatory effect of endogenous glucocorticoids. MIF has been demonstrated to be involved in a variety of inflammatory diseases. In this study, we examined the role of MIF in bleomycin (BLM)-induced lung injury and fibrosis. The levels of MIF in lung tissues and bronchoalveolar lavage fluids were significantly increased in the period 5–10 days after intratracheal administration of BLM. Treatment with the anti-MIF antibody significantly reduced the mortality at 14 days and the histopathological lung injury score at 10 days. These effects were accompanied with significant suppression of the accumulation of inflammatory cells in the alveolar space and tumor necrosis factor-α in the lungs at 7 days. However, the anti-MIF antibody did not affect either the content of lung hydroxyproline or the histopathological lung fibrosis score at 21 days after BLM. These data provide further evidence for the crucial role of MIF in acute lung inflammation but do not support the involvement of MIF in lung fibrosis induced by BLM in mice.

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