Loss of macrophage migration inhibitory factor impairs the growth properties of human HeLa cervical cancer cells

Xiao, Dingzhang; Dai, Bojie; Chen, J; Luo, Qiong; Liu, X Y; Lin, Qiaoli; Li, X H; Huang, Wenhui; Yu, Xin

doi:10.1111/j.1365-2184.2011.00787.x

Cited by 10 publications

(5 citation statements)

References 47 publications

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“…Further studies revealed that MIF transcription is induced by hypoxia-inducible factor 1 α (HIF1 α ) and is physically linked to HIF1 α through COP9 signalosome subunit 5 (CSN5) interaction [ 42 , 44 , 45 ]. MIF can potentially inhibit apoptosis and p53-mediated growth arrest and its depletion impairs cell proliferation in cancer [ 6 , 7 , 46 – 48 ]. It was suggested that MIF's action of blocking apoptosis is dependent on its catalytic oxidoreductase activity.…”

Section: Mif Structure and Functionmentioning

confidence: 99%

Brain Miffed by Macrophage Migration Inhibitory Factor

Savaskan

Fingerle‐Rowson

Buchfelder

et al. 2012

International Journal of Cell Biology

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Macrophage migration inhibitory factor (MIF) is a cytokine which also exhibits enzymatic properties like oxidoreductase and tautomerase. MIF plays a pivotal role in innate and acquired immunity as well as in the neuroendocrine axis. Since it is involved in the pathogenesis of acute and chronic inflammation, neoangiogenesis, and cancer, MIF and its signaling components are considered suitable targets for therapeutic intervention in several fields of medicine. In neurodegenerative and neurooncological diseases, MIF is a highly relevant, but still a hardly investigated mediator. MIF operates via intracellular protein-protein interaction as well as in CD74/CXCR2/CXCR4 receptor-mediated pathways to regulate essential cellular systems such as redox balance, HIF-1, and p53-mediated senescence and apoptosis as well as multiple signaling pathways. Acting as an endogenous glucocorticoid antagonist, MIF thus represents a relevant resistance gene in brain tumor therapies. Alongside this dual action, a functional homolog-annotated D-dopachrome tautomerase/MIF-2 has been uncovered utilizing the same cell surface receptor signaling cascade as MIF. Here we review MIF actions with respect to redox regulation in apoptosis and in tumor growth as well as its extracellular function with a focus on its potential role in brain diseases. We consider the possibility of MIF targeting in neurodegenerative processes and brain tumors by novel MIF-neutralizing approaches.

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Section: Mif Structure and Functionmentioning

confidence: 99%

Brain Miffed by Macrophage Migration Inhibitory Factor

Savaskan

Fingerle‐Rowson

Buchfelder

et al. 2012

International Journal of Cell Biology

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“…5 The knockdown of MIF also induced cell cycle arrest of G1/S transition and increased cell adhesion and therefore impaired their migratory capacity. 6 D-dopachrome tautomerase (D-DT) is the only known MIF homologue determined from human genome. It shares 38% amino acid identity with MIF, and its tertiary structures are remarkably similar.…”

mentioning

confidence: 99%

Combined Knockdown of D-dopachrome Tautomerase and Migration Inhibitory Factor Inhibits the Proliferation, Migration, and Invasion in Human Cervical Cancer

Wei

Zhang

2017

Int J Gynecol Cancer

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“…Although T cells are known as the main source of MIF production, other cell types including macrophages are also involved in MIF production and secretion. MIF is also considered as a proinflammatory cytokine with a range of targets which modulate the expression of a number of inflammatory molecules, including TNF-α, IL-6, IL-1b, IL-2, IL-8, and IFN-γ [Wang et al, 2012;Zhang et al, 2013] and playing an important immune regulatory role in several inflammatory diseases such as rheumatoid arthritis and atherosclerosis [Xiao et al, 2011;Saeedi et al, 2013].…”

Section: Introductionmentioning

confidence: 99%

Association between Macrophage Migration Inhibitory Factor Gene Variation and Response to Glucocorticoid Treatment in Sudden Sensorineural Hearing Loss

Yazdani¹,

Hamidi

Ghazavi³

et al. 2015

Audiol Neurotol

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Several lines of evidence suggest the role of the immune system in the pathogenesis of sudden sensorineural hearing loss (SSNHL). Macrophage migration inhibitory factor (MIF) mediates its role in various immune and inflammatory conditions by the regulation of immune reactions. Several studies have confirmed an association between MIF gene polymorphisms and susceptibility to various inflammatory and autoimmune disorders. The aim of this study was to explore the association between the MIF (-173 G/C) polymorphism (rs755622) and SSNHL in an Iranian population. In this case-control association study, SSNHL cases (n = 77) were included. Normal healthy subjects (n = 100) were also recruited from the same region. Genotyping for MIF (-173 G/C) polymorphism was carried out using the polymerase chain reaction-restriction fragment length polymorphism technique. The frequency of the MIF -173 C allele carriers (GC + CC genotype) was significantly elevated in SSNHL patients who responded to glucocorticoid treatment compared with the patients with no response to treatment. These results suggest that the MIF gene polymorphism is associated with a response to glucocorticoid treatment in patients with SSNHL.

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Loss of macrophage migration inhibitory factor impairs the growth properties of human HeLa cervical cancer cells

Abstract: MIF plays a pivotal role in proliferation and tumourigenesis of human HeLa cervical carcinoma cells, and may represent a promising therapeutic target for cancer intervention.

Cited by 10 publications

References 47 publications

Brain Miffed by Macrophage Migration Inhibitory Factor

Brain Miffed by Macrophage Migration Inhibitory Factor

Combined Knockdown of D-dopachrome Tautomerase and Migration Inhibitory Factor Inhibits the Proliferation, Migration, and Invasion in Human Cervical Cancer

Association between Macrophage Migration Inhibitory Factor Gene Variation and Response to Glucocorticoid Treatment in Sudden Sensorineural Hearing Loss

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