The role of macrophage inhibitory factor in tumorigenesis and central nervous system tumors

Bach, Jan-Philipp; Deuster, Oliver; Balzer‐Geldsetzer, Monika; Meyer, Bernhard; Dodel, Richard; Bacher, Michael

doi:10.1002/cncr.24245

Cited by 75 publications

(58 citation statements)

References 158 publications

(124 reference statements)

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“…MIF is a highly conserved multipotential protein that acts variously as a pro-inflammatory cytokine, a pituitary hormone, and as a cell proliferation and migration factor (Bifulco et al, 2008). It is a unique cytokine affecting multiple processes fundamental to tumorigenesis (Bach et al, 2009). In addition, MIF has prognostic value in human colorectal cancer because its expression correlates with aggressiveness of the cancer (Legendre et al 2003).…”

Section: Discussionmentioning

confidence: 99%

“…For further investigation on these transcripts we chose two highly represented genes, macrophage migration inhibitory factor (MIF) and metallothionein 2A (MT2A). They have recently been associated with tumorigenesis: MIF gene with tumor growth (Bifulco et al, 2008;Bach et al, 2009), and MT2A gene with breast cancer (Jin et al, 2004) and chemoresistance in ovarian cancers (L' Espe´rance et al, 2006). We examined whether the expression of MIF and MT2A is influenced by eIF3m in the HCT-116 cells.…”

Section: Identification Of Eif3m-associated Transcripts By Ribonomicsmentioning

confidence: 99%

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eIF3m expression influences the regulation of tumorigenesis-related genes in human colon cancer

Hong

et al. 2010

Oncogene

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Abnormal regulation of gene expression is essential for tumorigenesis. Recent studies indicate that regulation of oncogene expression and neoplastic transformation are controlled by subunits of eukaryotic translation initiation factors (eIFs). Here we focused on eIF3 performing a pivotal role in protein synthesis and the differential expression of its subunits in cancer. The most uncharacterized non-core subunit eIF3m was confirmed to be highly expressed in human cancer cell lines and colon cancer patient tissues. By expression silencing with eIF3m-specific small interfering RNA (siRNA), we confirmed that eIF3m influences cell proliferation, cell cycle progression and cell death in human colon cancer cell line HCT-116. Using a ribonomics approach, we identified a subset of elF3m-influenced genes and showed that the expression of two highly represented tumorigenesis-related genes, MIF and MT2, were affected by eIF3m at the mRNA level. We also confirmed eIF3m-dependent regulation of MT2A downstream molecule CDC25A, which is necessary for cell cycle progression in HCT-116 cells. These results suggest that eIF3m mediates regulation of tumorigenesis-related genes in human colon cancer. Further investigations on tumorigenesis-related genes and their regulation by eIFs will provide clues for designing targeted therapy for cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Identification Of Eif3m-associated Transcripts By Ribonomicsmentioning

confidence: 99%

eIF3m expression influences the regulation of tumorigenesis-related genes in human colon cancer

Hong

et al. 2010

Oncogene

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“…Despite its discovery in the mid-1960s as a T-cell-derived factor that modulated the motility of monocytes, macrophage migration inhibitory factor (MIF) has been shown to be involved in cancers [9][10][11][12][13]. Interestingly, both circulating and intracellular levels of MIF were elevated in patients with cancers, and the levels of MIF were closely correlated with tumor aggressiveness and metastatic potential, suggesting that MIF contributed to disease severity and survival [14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

Steroid receptor coactivator 3 regulates autophagy in breast cancer cells through macrophage migration inhibitory factor

et al. 2012

Cell Res

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SRC-3/AIB1 (steroid receptor coactivator 3/amplified in breast cancer 1) is an authentic oncogene that contributes to the development of drug resistance and poor disease-free survival in cancer patients. Autophagy is also an important cell death mechanism that has tumor suppressor function. In this study, we identified macrophage migration inhibitory factor (MIF) as a novel target gene of SRC-3 and demonstrated its importance in cell survival. Specifically, we showed that MIF is a strong suppressor of autophagic cell death. We further showed that suppression of MIF, in turn, induced autophagic cell death, enhanced chemosensitivity and inhibited tumorigenesis in a xenograft mouse tumorigenesis model. Our study demonstrated that regulation of MIF expression and suppression of autophagic cell death is a potent mechanism by which SRC-3 contributes to increased chemoresistance and tumorigenicity.

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“…Western blotting analysis of HUVEC cells lines showed higher MIF, ERK1, VEGF protein expression than in normal cholangiocytes. As described above, previous studies showed that MIF was overexpressed in multiple tumors, moreover, MIF was associated with blood-supply of cancer [11,12]. In addition, Fujiwaki et al found that expression of VEGF progressively increased in the progress of normal cervical epithelium→carcinoma in situ→invasive carcinoma [13].…”

Section: Discussionmentioning

confidence: 99%

MIF Promoted Cardiovascular Angiogenesis via Erk/Mapk Pathway

Cao¹,

Fan²,

Yu³

2017

J Clin Exp Cardiolog

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As the pivotal part of cardiovascular angiogenesis, endothelial cells dysfunction is the leading cause of cardiovascular diseases. Macrophage migration inhibitory factor (MIF) is a tumor growth factor with important roles in cervical tumor formation, invasion, progression and metastasis. However, there was no report on effect of MIF on endothelial cells is unclear, and it is still unknown whether MIF is associated with angiogenesis of endothelial cells. Our study was focused on the effect of MIF and PD98059 on endothelial cells HUVEC cell line, so as to investigate the influence of MIF on expression of vascular endothelial growth factor (VEGF). We also explored whether MIF will influence angiogenesis of endothelial cells via ERK/MAPK pathways. Endothelial cells HUVEC cells were conventionally cultured, and Western blot were used to detect the expression of MIF, ERK1 and VEGF proteins after HUVEC cells were intervened by MTT and PD98059. Inter-group difference was statistically assessed. Positive expressions of MIF, ERK1 and VEGF were observed in HUVEC cells. Proliferation activity in MIF group gradually increased after 24 h, 48 h or 72 h treatment (P<0.05). Expressions of ERK1 and VEGF were increased after MIF 48 h treatment (P<0.05). Proliferation activity in PD98059 group gradually decreased after 24 h, 48 h or 72 h treatment (P<0.05). Expressions of ERK1 and VEGF were decreased after MIF 48 h treatment (P<0.05). Compared with control group, expressions of ERK1, IL-2 and VEGF were significantly decreased in both MIF pre-stimulation +PD98059 inhibition group and PD98059 pre-exposure+MIF stimulation group (P<0.05), while no difference was observed between MIF pre-stimulation+PD98059 inhibition group and PD98059 pre-exposure+MIF stimulation group (P>0.05). Expressions of ERK1 and VEGF are involved in the process of endothelial cells HUVEC cell line. MIF is correlated with increased cell proliferation and promoted cardiovascular angiogenesis via ERK/MAPK pathway

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The role of macrophage inhibitory factor in tumorigenesis and central nervous system tumors

Cited by 75 publications

References 158 publications

eIF3m expression influences the regulation of tumorigenesis-related genes in human colon cancer

eIF3m expression influences the regulation of tumorigenesis-related genes in human colon cancer

Steroid receptor coactivator 3 regulates autophagy in breast cancer cells through macrophage migration inhibitory factor

MIF Promoted Cardiovascular Angiogenesis via Erk/Mapk Pathway

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