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Revisiting Neutrophil Gelatinase-Associated Lipocalin (NGAL) in Cancer: Saint or Sinner?

1,2,3,* and 1,2,3
1
INSERM UMRS 1138, Cell Death and Drug Resistance in Lymphoproliferative Disorders Team, Centre de Recherche des Cordeliers, 75006 Paris, France
2
Sorbonne Universités Paris Cité, F-75006 Paris, France
3
Université Paris Descartes, F-75005 Paris, France
*
Author to whom correspondence should be addressed.
Cancers 2018, 10(9), 336; https://doi.org/10.3390/cancers10090336
Received: 3 August 2018 / Revised: 13 September 2018 / Accepted: 15 September 2018 / Published: 18 September 2018
(This article belongs to the Special Issue Cancer Biomarkers)
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Abstract

Human neutrophil gelatinase-associated lipocalin (NGAL) is a glycoprotein present in a wide variety of tissues and cell types. NGAL exists as a 25 kDa monomer, a 46 kDa homodimer (the most abundant form in healthy subjects) and a 130 kDa disulfide-linked heterodimer bound to latent matrix metalloproteinase-9. Dysregulated expression of NGAL in human malignancies suggests its value as a clinical marker. A growing body of evidence is highlighting NGAL’s paradoxical (i.e., both beneficial and detrimental) effects on cellular processes associated with tumor development (proliferation, survival, migration, invasion, and multidrug resistance). At least two distinct cell surface receptors are identified for NGAL. This review (i) summarizes our current knowledge of NGAL’s expression profiles in solid tumors and leukemias, and (ii) critically evaluates the beneficial and detrimental activities of NGAL having been documented in a diverse range of cancer-derived cell lines. A better understanding of the causal relationships between NGAL dysregulation and tumor development will require a fine analysis of the molecular aspects and biological role(s) of NGAL both in primary tumors and at different stages of disease. Having an accurate picture of NGAL’s contribution to tumor progression is a prerequisite for attempting to modulate this protein as a putative therapeutic target. View Full-Text
Keywords: cancer; drug resistance; invasion; migration; matrix metalloproteinase-9; neutrophil gelatinase-associated lipocalin; signaling; survival cancer; drug resistance; invasion; migration; matrix metalloproteinase-9; neutrophil gelatinase-associated lipocalin; signaling; survival
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Bauvois, B.; Susin, S.A. Revisiting Neutrophil Gelatinase-Associated Lipocalin (NGAL) in Cancer: Saint or Sinner? Cancers 2018, 10, 336.

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