Correlation between the concentrations of lactoferrin and neutrophil gelatinase-associated lipocalin in meconium

Lisowska-Myjak, Barbara; Skarżyńska, Ewa; Wilczyńska, Paulina; Jakimiuk, Artur

doi:10.1007/s10534-017-0073-3

Cited by 6 publications

(6 citation statements)

References 22 publications

(31 reference statements)

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“…Two reports highlight a critical role of macrophage-secreted lipocalin-2 (LCN-2), a protein able to bind siderophore-complexed iron and to export it into the TME, in the promotion of cancer cells proliferation in vitro [ 91 , 92 ]. In the TAMs, LCN2 colocalizes with the iron-binding glycoprotein lactoferrin and promotes the release of pro-inflammatory cytokines into the TME [ 93 ]. LCN2 can also be released into the extracellular matrix where it binds to MMP-9, resulting in matrix degradation and EMT [ 92 , 94 ].…”

Section: Iron Handling By Tams and Its Implication For Cancer Progmentioning

confidence: 99%

Iron Metabolism in the Tumor Microenvironment—Implications for Anti-Cancer Immune Response

Sacco

Battaglia

Botta

et al. 2021

Cells

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New insights into the field of iron metabolism within the tumor microenvironment have been uncovered in recent years. Iron promotes the production of reactive oxygen species, which may either trigger ferroptosis cell death or contribute to malignant transformation. Once transformed, cancer cells divert tumor-infiltrating immune cells to satisfy their iron demand, thus affecting the tumor immunosurveillance. In this review, we highlight how the bioavailability of this metal shapes complex metabolic pathways within the tumor microenvironment and how this affects both tumor-associated macrophages and tumor-infiltrating lymphocytes functions. Furthermore, we discuss the potentials as well as the current clinical controversies surrounding the use of iron metabolism as a target for new anticancer treatments in two opposed conditions: (i) the “hot” tumors, which are usually enriched in immune cells infiltration and are extremely rich in iron availability within the microenvironment, and (ii) the “cold” tumors, which are often very poor in immune cells, mainly due to immune exclusion.

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Section: Iron Handling By Tams and Its Implication For Cancer Progmentioning

confidence: 99%

Iron Metabolism in the Tumor Microenvironment—Implications for Anti-Cancer Immune Response

Sacco

Battaglia

Botta

et al. 2021

Cells

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“…TAMs can secret Lcn2 and elevate intracellular iron concentration in tumor cells via Lcn2 as transporter [153]. In the TAMs, Lcn2 can colocalize with lactoferrin and release pro-inflammatory cytokines into the microenvironment [154]. It can also be stored as monomers or homodimers in the neutrophil-specific granules [155].…”

Section: Role Of Iron In Tumor Cell Biologymentioning

confidence: 99%

Iron Metabolism in Cancer

Wang

Ding

et al. 2018

IJMS

221

159

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Demanded as an essential trace element that supports cell growth and basic functions, iron can be harmful and cancerogenic though. By exchanging between its different oxidized forms, iron overload induces free radical formation, lipid peroxidation, DNA, and protein damages, leading to carcinogenesis or ferroptosis. Iron also plays profound roles in modulating tumor microenvironment and metastasis, maintaining genomic stability and controlling epigenetics. in order to meet the high requirement of iron, neoplastic cells have remodeled iron metabolism pathways, including acquisition, storage, and efflux, which makes manipulating iron homeostasis a considerable approach for cancer therapy. Several iron chelators and iron oxide nanoparticles (IONPs) has recently been developed for cancer intervention and presented considerable effects. This review summarizes some latest findings about iron metabolism function and regulation mechanism in cancer and the application of iron chelators and IONPs in cancer diagnosis and therapy.

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“…Indeed, meconium analysis has been used to establish an objective and comprehensive profile of drug and pesticide contact or use by the mother during pregnancy. 35,36 As such, the amount of PFASs remaining in the fetus can be inferred according to the concentration of PFASs in meconium, which is important to assess the health risk of prenatal exposure to PFASs for the fetus. However, few studies have assessed the elimination of PFASs through the human meconium.…”

Section: Introductionmentioning

confidence: 99%

Assessment of Fetal Exposure and Elimination of Perfluoroalkyl and Polyfluoroalkyl Substances: New Evidence from Paired Serum, Placenta, and Meconium Samples

Li,

Ma,

Qian

et al. 2024

Environ. Sci. Technol.

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Multiple pieces of evidence have shown that prenatal exposure to perfluoroalkyl and polyfluoroalkyl substances (PFASs) is closely related to adverse birth outcomes for infants. However, difficult access to human samples limits our understanding of PFASs transport and metabolism across the human placental barrier, as well as the accurate assessment of fetal PFASs exposure. Herein, we assess fetal exposure to 28 PFASs based on paired serum, placenta, and meconium samples. Overall, 21 PFASs were identified first to be exposed to the fetus prenatally and to be metabolized and excreted by the fetus. In meconium samples, 25 PFASs were detected, with perfluorooctane sulfonate and perfluorohexane sulfonic acid being the dominant congeners, suggesting the metabolism and excretion of PFASs through meconium. Perfluoroalkyl sulfonic acids might be more easily eliminated through the meconium than perfluorinated carboxylic acids. Importantly, based on molecular docking, MRP1, OATP2B1, ASCT1, and P-gp were identified as crucial transporters in the dynamic placental transfer of PFASs between the mother and the fetus. ATSC5p and PubchemFP679 were recognized as critical structural features that affect the metabolism and secretion of PFASs through meconium. With increasing carbon chain length, both the transplacental transfer efficiency and meconium excretion efficiency of PFASs showed a structure-dependent manner. This study reports, for the first time, that meconium, which is a noninvasive and stable biological matrix, can be strong evidence of prenatal PFASs exposure.

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Correlation between the concentrations of lactoferrin and neutrophil gelatinase-associated lipocalin in meconium

Cited by 6 publications

References 22 publications

Iron Metabolism in the Tumor Microenvironment—Implications for Anti-Cancer Immune Response

Iron Metabolism in the Tumor Microenvironment—Implications for Anti-Cancer Immune Response

Iron Metabolism in Cancer

Assessment of Fetal Exposure and Elimination of Perfluoroalkyl and Polyfluoroalkyl Substances: New Evidence from Paired Serum, Placenta, and Meconium Samples

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