Expression of Macrophage Migration Inhibitory Factor and CD74 in Cervical Squamous Cell Carcinoma

Cheng, Ruochuan; Deng, Weiguo; Niu, Chen; Li, Yi-yang; Fu, Yan

doi:10.1097/igc.0b013e31821c45b7

Cited by 38 publications

(38 citation statements)

References 18 publications

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“…ISO-1[(S, R)-3-(4-hydroxyphenyl)-4, 5-dihydro-5-isoxazole acetic acid methyl ester)], a prototype inhibitor of MIF (Al-Abed & VanPatten, 2011), reduced the tumor size and angiogenesis in the mouse xenograft model of DU-145 prostate cancer (Meyer-Siegler et al, 2006). MIF and CD74, through their over-expression, are known to enhance VEGF's expression in cervical cancer (Cheng et al, 2011). In neuroblastoma, N-myc expression is linked with advanced stage (Ren et al, 2004).…”

Section: Mif and Angiogenesismentioning

confidence: 99%

Macrophage Migration Inhibitory Factor: a Potential Marker for Cancer Diagnosis and Therapy

Babu¹,

Chetal²,

Kumar³

2012

Asian Pacific Journal of Cancer Prevention

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Macrophage migration inhibitory factor (MIF) is a pluripotent cytokine which plays roles in inflammation, immune responses and cancer development. It assists macrophages in carrying out functions like phagocytosis, adherence and motility. Of late, MIF is implicated in almost all stages of neoplasia and expression is a feature of most types of cancer. The presence of MIF in almost all tumors and all stages of cancer makes it an interesting candidate for cancer therapy. This review explores the roles of MIF in neoplasia.

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Section: Mif and Angiogenesismentioning

confidence: 99%

Macrophage Migration Inhibitory Factor: a Potential Marker for Cancer Diagnosis and Therapy

Babu¹,

Chetal²,

Kumar³

2012

Asian Pacific Journal of Cancer Prevention

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“…As an important proinflammatory cytokine, MIF can counteract glucocorticoid signaling by activating immune or inflammatory cells and promoting inflammatory cytokine release [9]. Moreover, MIF has been shown to induce various pathologic events, such as acute respiratory distress syndrome [15], arthritis [22], glomerulonephritis [20], and angiogenesis [12,30]. Moreover, Type 1 Modic changes of cartilage end plates are characterized by an inflammatory reaction, but to our knowledge, the relationship between MIF and cartilage end plates with Type 1 Modic changes has not been investigated.…”

Section: Introductionmentioning

confidence: 99%

Migration Inhibitory Factor Enhances Inflammation via CD74 in Cartilage End Plates with Modic Type 1 Changes on MRI

Xiong

Huang

Cun

et al. 2014

Clinical Orthopaedics &Amp; Related Research

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Background Type 1 Modic changes are characterized by edema, vascularization, and inflammation, which lead to intervertebral disc degeneration. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine closely related to the inflammatory cytokines detected in degenerative intervertebral disc tissues. However, the existence and role of MIF and its receptor CD74 in intervertebral disc degeneration have not been elucidated. Questions/purposes We asked whether (1) MIF and its receptor CD74 are expressed in cartilage end plates with Type 1 Modic changes, (2) MIF is associated with cartilage end plate degeneration, (3) the MIF antagonist (S, R)-3(4-hydroxyphenyl)-4, 5-dihydro-5-isoxazole acetic acid methyl ester (ISO-1) suppresses MIF-induced inflammatory cytokine release, and (4) inflammatory cytokines are released by cartilage end plate chondrocytes via CD74 by activating the CD74 antibody (CD74Ab). Methods We examined MIF and CD74 expression by human cartilage end plate chondrocytes and tissues with Type 1 Modic changes from eight patients using immunocytofluorescence and immunohistochemistry. MIF production by the chondrocytes was assessed by ELISA and PCR. We compared cytokine release by chondrocytes treated with MIF in the presence or absence of exogenous ISO-1 by ELISA. Cytokine release by chondrocytes after treatment with CD74Ab was determined by ELISA. Results MIF was expressed in degenerated human cartilage end plate tissues and chondrocytes. Lipopolysaccharide and tumor necrosis factor a (TNF-a) upregulated MIF expression and increased MIF secretion in chondrocytes in a dose-dependent manner. MIF increased the secretion of IL-6, IL-8, and prostaglandin E2 (PGE2) in a dose-dependent manner. ISO-1 reduced the secretion of IL-6, IL-8, and PGE2. CD74Ab activated CD74 and induced release of inflammatory cytokines. Conclusions Chondrocytes in cartilage end plate with Type 1 Modic changes express MIF and its receptor CD74.

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“…Previous study showed that MIF induced VEGF secretion in a dose-dependent manner in cervical cancer cells, which could be inhibited by anti-CD74 antibody (Cheng et al 2011a). To study the effects on VEGF secretion in thyroid cancer, BCPAP and K1 cells were treated with the same experimental protocol previously used.…”

Section: Decreased Vegf Secretion With Anti-cd74 Antibody Treatmentmentioning

confidence: 99%

“…This ligand-receptor interaction may be an important link between chronic inflammation and carcinogenesis (Bucala & Donnelly 2007). The expression of MIF and/or CD74 has been explored in several forms of cancer (Ren et al 2005, Xu et al 2008, Nagata et al 2009, Cheng et al 2011a). In addition, MIF has been identified as a hypoxia-induced gene, and its expression serves to activate a proangiogenic transcriptional program (Winner et al 2007).…”

Section: Introductionmentioning

confidence: 99%

CD74 expression and its therapeutic potential in thyroid carcinoma

Cheng¹,

Liu²,

Chen³

et al. 2015

Endocrine-Related Cancer

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CD74, the invariant chain of major histocompatibility complex class II, is also a receptor for macrophage migration inhibitory factor (MIF). CD74 and MIF have been associated with tumor progression and metastasis in hematologic and solid tumors. In this study, we found that 60 and 65% of papillary thyroid cancers were positive for CD74 and MIF immunohistochemical staining respectively. Anaplastic thyroid cancer was negative for MIF, but mostly positive for CD74 expression. Normal thyroid tissue and follicular adenomas were negative for CD74 expression. CD74 expression in papillary thyroid cancer was associated with larger tumor size (PZ0.043), extrathyroidal invasion (PZ0.021), advanced TNM stage (PZ0.006), and higher MACIS score (PZ0.026). No clinicopathological parameter was associated with MIF expression. Treatment with anti-CD74 antibody in thyroid cancer cells inhibited cell growth, colony formation, cell migration and invasion, and vascular endothelial growth factor secretion. In contrast, treatment with recombinant MIF induced an increase in cell invasion. Anti-CD74 treatment reduced AKT phosphorylation and stimulated AMPK activation. Our findings suggest that CD74 overexpression in thyroid cancer is associated with advanced tumor stage and may serve as a therapeutic target.

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Expression of Macrophage Migration Inhibitory Factor and CD74 in Cervical Squamous Cell Carcinoma

Abstract: Overexpression of MIF and CD74 in SCC and its precancerous lesions and the up-regulation of VEGF secretion in cervical cancer cells indicate that MIF and CD74 may play critical roles in the pathogenesis and angiogenesis of cervical cancer.

Cited by 38 publications

References 18 publications

Macrophage Migration Inhibitory Factor: a Potential Marker for Cancer Diagnosis and Therapy

Macrophage Migration Inhibitory Factor: a Potential Marker for Cancer Diagnosis and Therapy

Migration Inhibitory Factor Enhances Inflammation via CD74 in Cartilage End Plates with Modic Type 1 Changes on MRI

CD74 expression and its therapeutic potential in thyroid carcinoma

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