Interference of Macrophage Migration Inhibitory Factor Expression in a Mouse Melanoma Inhibits Tumor Establishment by Up-Regulating Thrombospondin-1

Culp, W. David; Tsagozis, Panagiotis; Burgio, Michael; Russell, Paul; Pisa, Pavel; Garland, Donita

doi:10.1158/1541-7786.mcr-07-0229

Cited by 11 publications

(16 citation statements)

References 35 publications

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“…14,15 In lung cancer MIF expression is associated with increased production of angiogenic CXC chemokines both in vitro, 16 and in vivo.…”

Section: Discussionmentioning

confidence: 99%

“…We and others have shown that MIF is markedly overexpressed in lung cancer [1][2][3] and nearly all other common solid tumors; eg, breast, 4 -8 ovarian, 9,10 prostate, 6 -8 bladder, 11,12 and colon cancer, 13 as well as melanoma. 14,15 In lung cancer MIF expression is associated with increased production of angiogenic CXC chemokines both in vitro, 16 and in vivo. 2 High expression of MIF in patients with lung cancer is also associated with a worse prognosis for disease-free and overall survival.…”

mentioning

confidence: 99%

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Expression of CD74, the Receptor for Macrophage Migration Inhibitory Factor, in Non-Small Cell Lung Cancer

McClelland

Zhao

Carskadon

et al. 2009

The American Journal of Pathology

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Macrophage migration inhibitory factor (MIF) is a multifunctional cytokine that is overexpressed in lung cancer. The MIF receptor was recently discovered and found to be the invariant chain of the HLA class II molecule, CD74. We hypothesized that the expression of this receptor-ligand pair in lung cancer is associated with the angiogenic activity and level of CXC chemokine expression in human specimens of non-small cell lung cancer. We, therefore, performed immunolocalization of CD74 and compared it with the localization of MIF in non-small cell lung cancer to determine their respective locations, as well as the relationship between the co-expression of MIF-CD74 and angiogenic CXC chemokines with tumor angiogenesis. We found intense CD74 expression by immunohistochemistry in 57 of 70 tumors with minimal to no staining in the remaining 13 tumors. Comparing the localization of CD74 with its putative ligand, MIF, we found that CD74 and MIF were co-expressed in tumors in close proximity, and that co-expression of the MIF-CD74 pair was associated with both higher levels of tumor-associated angiogenic CXC chemokines (ie, the ELR score) and greater vascularity compared with tumors in which MIF-CD74 co-expression was not present. We also found that MIF induced angiogenic CXC chemokine expression in an autocrine manner in vitro , a function that was specifically inhibited by antibodies to CD74. (Am J Pathol

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“…14,15 In lung cancer MIF expression is associated with increased production of angiogenic CXC chemokines both in vitro, 16 and in vivo.…”

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Expression of CD74, the Receptor for Macrophage Migration Inhibitory Factor, in Non-Small Cell Lung Cancer

McClelland

Zhao

Carskadon

et al. 2009

The American Journal of Pathology

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“…Finally, several recent reports have described MIF to activate HIF-1α under hypoxic conditions [78]; this serves to activate a pro-angiogenic transcriptional program that is necessary for tumor progression. MIF downregulates the NK cell receptor NKG2D, as mentioned above, thereby impairing NK cell cytoxicity toward tumor cells [67] and it upregulates the anti-angiogenic factor thrombospondin-1 [79]. Nevertheless, the precise molecular mechanisms by which MIF mediates tumorigenesis in particular tumor types remain to be more precisely elucidated.…”

Section: Mif In Cancermentioning

confidence: 99%

Macrophage migration inhibitory factor (MIF): A promising biomarker

Grieb¹,

Merk²,

Bernhagen³

et al. 2010

Drug News &Amp; Perspectives

189

171

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Macrophage migration inhibitory (MIF) factor is an immunoregulatory cytokine whose effect on arresting random immune cell movement was recognized several decades ago. Despite its historic name, MIF also has a direct chemokine-like function and promotes cell recruitment. Multiple clinical studies have pointed to the utility of MIF as a biomarker for different diseases that have an inflammatory component; these include systemic infections and sepsis, autoimmune diseases, cancer, and metabolic disorders such as type 2 diabetes and obesity. The identification of functional promoter polymorphisms in the MIF gene (MIF) and their association with the susceptibility or severity of different diseases has served not only to validate MIF’s role in disease development but opened the possibility of using MIF genotype information to better predict risk and outcome. In this article, we review the clinical data of MIF and discuss its potential as a biomarker for different disease applications.

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“…B16 melanoma cells express very low levels of TSP1 mRNA, and TSP1 protein was reported to be below detectable levels. 37 When the tumors obtained a volume of 200 mm 3 , half of the mice of Figure 6. TSP1 and CD47 modulate irradiated hindlimb responses to vasoactive challenge.…”

Section: Absence Of Endogenous Tsp1 Does Not Limit Tumor Response To mentioning

confidence: 99%

Thrombospondin-1 and CD47 Limit Cell and Tissue Survival of Radiation Injury

Isenberg

Maxhimer

Hyodo

et al. 2008

The American Journal of Pathology

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Radiation, a primary mode of cancer therapy, acutely damages cellular macromolecules and DNA and elicits stress responses that lead to cell death. The known cytoprotective activity of nitric oxide (NO) is blocked by thrombospondin-1, a potent antagonist of NO/ cGMP signaling in ischemic soft tissues, suggesting that thrombospondin-1 signaling via its receptor CD47 could correspondingly increase radiosensitivity. We show here that soft tissues in thrombospondin-1-null mice are remarkably resistant to radiation injury. Twelve hours after 25-Gy hindlimb irradiation, thrombospondin-1-null mice showed significantly less cell death in both muscle and bone marrow. Two months after irradiation, skin and muscle units in null mice showed minimal histological evidence of radiation injury and near full retention of mitochondrial function. Additionally , both tissue perfusion and acute vascular responses to NO were preserved in irradiated thrombospondin-1-null hindlimbs. The role of thrombospondin-1 in radiosensitization is specific because thrombospondin-2-null mice were not protected. However , mice lacking CD47 showed radioresistance similar to thrombospondin-1-null mice. Both thrombospondin-1-and CD47-dependent radiosensitization is cell autonomous because vascular cells isolated from the respective null mice showed dramatically increased survival and improved proliferative capacity after irradiation in vitro. Therefore , thrombospondin-1/CD47 antagonists may have selective radioprotective activity for normal tissues.

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Interference of Macrophage Migration Inhibitory Factor Expression in a Mouse Melanoma Inhibits Tumor Establishment by Up-Regulating Thrombospondin-1

Cited by 11 publications

References 35 publications

Expression of CD74, the Receptor for Macrophage Migration Inhibitory Factor, in Non-Small Cell Lung Cancer

Expression of CD74, the Receptor for Macrophage Migration Inhibitory Factor, in Non-Small Cell Lung Cancer

Macrophage migration inhibitory factor (MIF): A promising biomarker

Thrombospondin-1 and CD47 Limit Cell and Tissue Survival of Radiation Injury

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