Knockdown of macrophage migration inhibitory factor (MIF), a novel target to protect neurons from parthanatos induced by simulated post-spinal cord injury oxidative stress

Yang, Dongfang; Shu, Tingting; Zhao, Haosen; Sun, Yang; Xu, Weibing; Tu, Guanjun

doi:10.1016/j.bbrc.2019.12.115

Cited by 32 publications

(23 citation statements)

References 40 publications

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“…On the other hand, the occurrence of parthanatos mainly comes from the abnormal activation of PARP-1, so it can also lead to the occurrence of parthanatos in tumor cells by enhancing the activity of PARP-1 to inhibit the proliferation of tumor cells. Because PARP-1 is involved in many DNA repair pathways and the maintenance of genomic stability, 390 the regulation of PARP-1 activity is an important means for the clinical treatment of related cancers. Breast cancer proteins, especially BRCA1 and BRCA2, participate in homologous recombination repair (HRR).…”

Section: Pyroptosis Signaling Pathways In Cancermentioning

confidence: 99%

Regulated cell death (RCD) in cancer: key pathways and targeted therapies

Liao

Qin

et al. 2022

Sig Transduct Target Ther

388

154

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Regulated cell death (RCD), also well-known as programmed cell death (PCD), refers to the form of cell death that can be regulated by a variety of biomacromolecules, which is distinctive from accidental cell death (ACD). Accumulating evidence has revealed that RCD subroutines are the key features of tumorigenesis, which may ultimately lead to the establishment of different potential therapeutic strategies. Hitherto, targeting the subroutines of RCD with pharmacological small-molecule compounds has been emerging as a promising therapeutic avenue, which has rapidly progressed in many types of human cancers. Thus, in this review, we focus on summarizing not only the key apoptotic and autophagy-dependent cell death signaling pathways, but the crucial pathways of other RCD subroutines, including necroptosis, pyroptosis, ferroptosis, parthanatos, entosis, NETosis and lysosome-dependent cell death (LCD) in cancer. Moreover, we further discuss the current situation of several small-molecule compounds targeting the different RCD subroutines to improve cancer treatment, such as single-target, dual or multiple-target small-molecule compounds, drug combinations, and some new emerging therapeutic strategies that would together shed new light on future directions to attack cancer cell vulnerabilities with small-molecule drugs targeting RCD for therapeutic purposes.

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Section: Pyroptosis Signaling Pathways In Cancermentioning

confidence: 99%

Regulated cell death (RCD) in cancer: key pathways and targeted therapies

Liao

Qin

et al. 2022

Sig Transduct Target Ther

388

154

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“…Inhibition of MIF's nuclease activity by mutation of its nuclease domain or by disruption of its protein–protein interaction with AIF markedly attenuated ischemic neuronal cell death and acute brain injury in mice. This interaction between MIF and AIF was confirmed by another study which showed MIF knockdown protected neurons from oxidative stress-induced parthanatos associated with spinal cord injury [ 62 ]. In this regard, it would be interesting to determine whether cytosolic MIF contributes to DNA damage in other types of cell injuries too.…”

Section: Intracellular Partnersmentioning

confidence: 53%

“…In contrast, in a model of transient middle cerebral artery occlusion, MIF was found to contribute to stroke pathology in mice and neuronal death in vitro, with knockout of MIF or administration of MIF antagonist ISO-1 resulting in a smaller infarct size [ 17 , 125 , 126 ]. In addition, MIF was recently found to act as a nuclease and thereby contributes to ischemic neuronal cell death [ 13 , 62 ]. Together, these data suggest a detrimental role for MIF in brain ischemia.…”

Section: Tissue Injurymentioning

confidence: 99%

Macrophage migration inhibitory factor family proteins are multitasking cytokines in tissue injury

Song

Xiao

Poelarends

et al. 2022

Cell. Mol. Life Sci.

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The family of macrophage migration inhibitory factor (MIF) proteins in humans consist of MIF, its functional homolog D-dopachrome tautomerase (D-DT, also known as MIF-2) and the relatively unknown protein named DDT-like (DDTL). MIF is a pleiotropic cytokine with multiple properties in tissue homeostasis and pathology. MIF was initially found to associate with inflammatory responses and therefore established a reputation as a pro-inflammatory cytokine. However, increasing evidence demonstrates that MIF influences many different intra- and extracellular molecular processes important for the maintenance of cellular homeostasis, such as promotion of cellular survival, antioxidant signaling, and wound repair. In contrast, studies on D-DT are scarce and on DDTL almost nonexistent and their functions remain to be further investigated as it is yet unclear how similar they are compared to MIF. Importantly, the many and sometimes opposing functions of MIF suggest that targeting MIF therapeutically should be considered carefully, taking into account timing and severity of tissue injury. In this review, we focus on the latest discoveries regarding the role of MIF family members in tissue injury, inflammation and repair, and highlight the possibilities of interventions with therapeutics targeting or mimicking MIF family proteins.

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“…Therefore, MIF possesses nuclease activity that is critical for PARP-1-dependent DNA damage and cell death in the parthanatos pathway. Another study showed that MIF knockdown enabled neuronal protection against parthanatos under conditions of simulated in vivo oxidative stress after spinal cord injury (SCI) [43]. Inhibition of MIF nuclease activity is a possible treatment target in diseases induced by PARP-1 overactivation [42,43].…”

Section: Mif Structure and Functionmentioning

confidence: 99%

Nematode Orthologs of Macrophage Migration Inhibitory Factor (MIF) as Modulators of the Host Immune Response and Potential Therapeutic Targets

et al. 2022

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One of the adaptations of nematodes, which allows long-term survival in the host, is the production of proteins with immunomodulatory properties. The parasites secrete numerous homologs of human immune mediators, such as macrophage migration inhibitory factor (MIF), which is a substantial regulator of the inflammatory immune response. Homologs of mammalian MIF have been recognized in many species of nematode parasites, but their role has not been fully understood. The application of molecular biology and genetic engineering methods, including the production of recombinant proteins, has enabled better characterization of their structure and properties. This review provides insight into the current state of knowledge on MIF homologs produced by nematodes, as well as their structure, enzymatic activity, tissue expression pattern, impact on the host immune system, and potential use in the treatment of parasitic, inflammatory, and autoimmune diseases.

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Knockdown of macrophage migration inhibitory factor (MIF), a novel target to protect neurons from parthanatos induced by simulated post-spinal cord injury oxidative stress

Cited by 32 publications

References 40 publications

Regulated cell death (RCD) in cancer: key pathways and targeted therapies

Regulated cell death (RCD) in cancer: key pathways and targeted therapies

Macrophage migration inhibitory factor family proteins are multitasking cytokines in tissue injury

Nematode Orthologs of Macrophage Migration Inhibitory Factor (MIF) as Modulators of the Host Immune Response and Potential Therapeutic Targets

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