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Cell Death in Biology and Diseases

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 October 2020) | Viewed by 54071

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Dr. Peter Richter

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Guest Editor

Gravitational Biology Group, Department of Biology, Cell Biology Division, Friedrich-Alexander-Universität Erlangen-Nürnberg, 91058 Erlangen, Germany
Interests: cell biology; plant physiology; photodynamic therapy
Special Issues, Collections and Topics in MDPI journals

Dr. Marcus Krüger

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Co-Guest Editor

Environmental Cell Biology Group, Department of Microgravity and Translational Regenerative Medicine, Otto von Guericke University, 39106 Magdeburg, Germany
Interests: cell biology; cancer biology; environmental influences; microgravity; cellular communication; photodynamic therapy; cancer treatment; antimicrobial resistance; tumor microbiome
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cell death is a major biological phenomenon. Like other cellular processes (e.g., cell proliferation or cell differentiation), cell death is a choice that a cell has to make—sometimes voluntarily, other times accidentally. Cell death serves a purpose in the biology of multicellular organisms. However, the machinery for cell death is evolutionarily conserved and the elements can also be found in single-celled organisms. The molecular mechanisms of cell death (or conversely cell survival) are complex and often closely connected to other cellular processes, such as cell proliferation or differentiation and thus part of a broad signaling network. The disruption of these mechanisms often causes developmental abnormalities, and factors that trigger cell death can directly contribute to the pathogenesis of many diseases, including cancer, neurodegenerative diseases, and tissue injury. Additionally, in plants programmed cell death plays an important role in the formation of sclerenchyma as well as xylem (water and mineral transport).

The exploration of the role of cell death in disease development as well as the modulation of cell death for treatment of diseases demands a constant update of our knowledge. This Special Issue highly welcomes original research articles, short communications, and review manuscripts. Interdisciplinary contributions will help to get a detailed overview of this exciting research field in medicine, pest control, and other areas, providing great opportunities for new discoveries and applications in life science.

Dr. Peter Richter
Dr. Marcus Krüger
Guest Editors

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

programmed cell death
apoptosis
necrosis
autoimmune diseases
cancer research
pharmacognosy
photodynamic therapy
immune system

Published Papers (13 papers)

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Editorial

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5 pages, 680 KiB

Open AccessEditorial

Remove, Refine, Reduce: Cell Death in Biological Systems

by Marcus Krüger

Int. J. Mol. Sci. 2023, 24(8), 7028; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24087028 - 10 Apr 2023

Cited by 1 | Viewed by 934

Abstract

Cell death is an important biological phenomenon [...] Full article

(This article belongs to the Special Issue Cell Death in Biology and Diseases)

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Research

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12 pages, 4473 KiB

Open AccessArticle

Polyhexamethylene Guanidine Phosphate Induces Apoptosis through Endoplasmic Reticulum Stress in Lung Epithelial Cells

by Mi Ho Jeong, Mi Seon Jeon, Ga Eun Kim and Ha Ryong Kim

Int. J. Mol. Sci. 2021, 22(3), 1215; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031215 - 26 Jan 2021

Cited by 11 | Viewed by 2374

Abstract

Airway epithelial cell death contributes to the pathogenesis of lung fibrosis. Polyhexamethylene guanidine phosphate (PHMG-p), commonly used as a disinfectant, has been shown to be strongly associated with lung fibrosis in epidemiological and toxicological studies. However, the molecular mechanism underlying PHMG-p-induced epithelial cell death is currently unclear. We synthesized a PHMG-p–fluorescein isothiocyanate (FITC) conjugate and assessed its uptake into lung epithelial A549 cells. To examine intracellular localization, the cells were treated with PHMG-p–FITC; then, the cytoplasmic organelles were counterstained and observed with confocal microscopy. Additionally, the organelle-specific cell death pathway was investigated in cells treated with PHMG-p. PHMG-p–FITC co-localized with the endoplasmic reticulum (ER), and PHMG-p induced ER stress in A549 cells and mice. The ER stress inhibitor tauroursodeoxycholic acid (TUDCA) was used as a pre-treatment to verify the role of ER stress in PHMG-p-induced cytotoxicity. The cells treated with PHMG-p showed apoptosis, which was inhibited by TUDCA. Our results indicate that PHMG-p is rapidly located in the ER and causes ER-stress-mediated apoptosis, which is an initial step in PHMG-p-induced lung fibrosis. Full article

(This article belongs to the Special Issue Cell Death in Biology and Diseases)

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14 pages, 3683 KiB

Open AccessArticle

Hepatocyte-Derived Igκ Exerts a Protective Effect against ConA-Induced Acute Liver Injury

by Sha Yin, Qianwen Shi, Wenwei Shao, Chi Zhang, Yixiao Zhang, Xiaoyan Qiu and Jing Huang

Int. J. Mol. Sci. 2020, 21(24), 9379; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21249379 - 09 Dec 2020

Cited by 5 | Viewed by 2344

Abstract

Immunoglobulin (Igκ) has been reported to be expressed in sorted liver epithelial cells of μMT mice, and the sequence characteristics of hepatocyte-derived Igκ were different from those of classical B-cell-derived Igκ. However, the physiological function of hepatocyte-derived Igκ is still unclear. The expression of Igκ was firstly identified in primary hepatocytes and normal liver cell line (NCTC1469), and hepatocyte-derived Igκ expression was elevated and displayed unique localization in hepatocytes of concanavalin A (ConA)-induced hepatitis model. Moreover, Igκ knockout mice were more sensitive to ConA-induced hepatitis and had higher serum aspartate aminotransferase (AST) levels, more severe histological injury and a greater number of terminal deoxynucleotide transferase-mediated deoxyuridine triphosphate nick end-labeling (TUNEL)-positive cells as compared with littermate controls. Furthermore, knockdown of Igκ in primary hepatocytes and NCTC1469 cells led to accelerated activation of the mitochondrial death pathway and caspase-3 cleavage in vitro, which might be related to inhibition of NF-κB signaling pathway and activation of JNK via the cytoskeleton dynamics. Taken together, these results indicate that hepatocyte-derived Igκ mediates cellular resistance to ConA-induced liver injury by inhibiting activation of caspase-3 and the mitochondrial death pathway, suggesting that Igκ plays an important role in hepatocyte survival and exerts a protective effect against ConA-induced liver injury in mice. Full article

(This article belongs to the Special Issue Cell Death in Biology and Diseases)

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12 pages, 2925 KiB

Open AccessArticle

TNF Is Partially Required for Cell-Death-Triggered Skin Inflammation upon Acute Loss of cFLIP

by Maria Feoktistova, Roman Makarov, Martin Leverkus, Amir S. Yazdi and Diana Panayotova-Dimitrova

Int. J. Mol. Sci. 2020, 21(22), 8859; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21228859 - 23 Nov 2020

Cited by 6 | Viewed by 2079

Abstract

cFLIP is required for epidermal integrity and skin inflammation silencing via protection from TNF-induced keratinocyte apoptosis. Here, we generated and analyzed cFLIP epidermal KO mice with additional TNF deficiency. Intriguingly, the ablation of TNF rescued the pathological phenotype of epidermal cFLIP KO from characteristic weight loss and increased mortality. Moreover, the lack of TNF in these animals strongly reduced and delayed the epidermal hyperkeratosis and the increased apoptosis in keratinocytes. Our data demonstrate that TNF signaling in cFLIP-deficient keratinocytes is the critical factor for the regulation of skin inflammation via modulated cytokine and chemokine expression and, thus, the attraction of immune cells. Our data suggest that autocrine TNF loop activation upon cFLIP deletion is dispensable for T cells, but is critical for neutrophil attraction. Our findings provide evidence for a negative regulatory role of cFLIP for TNF-dependent apoptosis and partially for epidermal inflammation. However, alternative signaling pathways may contribute to the development of the dramatic skin disease upon cFLIP deletion. Our data warrant future studies of the regulatory mechanism controlling the development of skin disease upon cFLIP deficiency and the role of cFLIP/TNF in a number of inflammatory skin diseases, including toxic epidermal necrolysis (TEN). Full article

(This article belongs to the Special Issue Cell Death in Biology and Diseases)

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11 pages, 2416 KiB

Open AccessArticle

tert-Butyl Hydroperoxide (tBHP)-Induced Lipid Peroxidation and Embryonic Defects Resemble Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency in C. elegans

by Hung-Chi Yang, Hsiang Yu, Tian-Hsiang Ma, Wen-Ye Tjong, Arnold Stern and Daniel Tsun-Yee Chiu

Int. J. Mol. Sci. 2020, 21(22), 8688; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21228688 - 18 Nov 2020

Cited by 9 | Viewed by 2651

Abstract

G6PD is required for embryonic development in animals, as severe G6PD deficiency is lethal to mice, zebrafish and nematode. Lipid peroxidation is linked to membrane-associated embryonic defects in Caenorhabditis elegans (C. elegans). However, the direct link between lipid peroxidation and embryonic lethality has not been established. The aim of this study was to delineate the role of lipid peroxidation in gspd-1-knockdown (ortholog of g6pd) C. elegans during reproduction. tert-butyl hydroperoxide (tBHP) was used as an exogenous inducer. Short-term tBHP administration reduced brood size and enhanced germ cell death in C. elegans. The altered phenotypes caused by tBHP resembled GSPD-1 deficiency in C. elegans. Mechanistically, tBHP-induced malondialdehyde (MDA) production and stimulated calcium-independent phospholipase A₂ (iPLA) activity, leading to disturbed oogenesis and embryogenesis. The current study provides strong evidence to support the notion that enhanced lipid peroxidation in G6PD deficiency promotes death of germ cells and impairs embryogenesis in C. elegans. Full article

(This article belongs to the Special Issue Cell Death in Biology and Diseases)

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23 pages, 5221 KiB

Open AccessArticle

Cell Death Mechanisms Induced by CLytA-DAAO Chimeric Enzyme in Human Tumor Cell Lines

by María Fuentes-Baile, Pilar García-Morales, Elizabeth Pérez-Valenciano, María P. Ventero, Jesús M. Sanz, Camino de Juan Romero, Víctor M. Barberá, Cristina Alenda and Miguel Saceda

Int. J. Mol. Sci. 2020, 21(22), 8522; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21228522 - 12 Nov 2020

Cited by 8 | Viewed by 1953

Abstract

The combination of the choline binding domain of the amidase N-acetylmuramoyl-L-alanine (CLytA)-D-amino acid oxidase (DAAO) (CLytA-DAAO) and D-Alanine induces cell death in several pancreatic and colorectal carcinoma and glioblastoma cell lines. In glioblastoma cell lines, CLytA-DAAO-induced cell death was inhibited by a pan-caspase inhibitor, suggesting a classical apoptotic cell death. Meanwhile, the cell death induced in pancreatic and colon carcinoma cell lines is some type of programmed necrosis. In this article, we studied the mechanisms that trigger CLytA-DAAO-induced cell death in pancreatic and colorectal carcinoma and glioblastoma cell lines and we acquire a further insight into the necrotic cell death induced in pancreatic and colorectal carcinoma cell lines. We have analyzed the intracellular calcium mobilization, mitochondrial membrane potential, PARP-1 participation and AIF translocation. Although the mitochondrial membrane depolarization plays a crucial role, our results suggest that CLytA-DAAO-induced cell death is context dependent. We have previously detected pancreatic and colorectal carcinoma cell lines (Hs766T and HT-29, respectively) that were resistant to CLytA-DAAO-induced cell death. In this study, we have examined the putative mechanism underlying the resistance in these cell lines, evaluating both detoxification mechanisms and the inflammatory and survival responses. Overall, our results provide a better understanding on the cell death mechanism induced by CLytA-DAAO, a promising therapy against cancer. Full article

(This article belongs to the Special Issue Cell Death in Biology and Diseases)

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19 pages, 5636 KiB

Open AccessArticle

Pygenic Acid A (PA) Sensitizes Metastatic Breast Cancer Cells to Anoikis and Inhibits Metastasis In Vivo

by Ga-Eun Lim, Jee Young Sung, Suyeun Yu, Younmi Kim, Jaegal Shim, Hyo Jung Kim, Myoung Lae Cho, Jae-Seon Lee and Yong-Nyun Kim

Int. J. Mol. Sci. 2020, 21(22), 8444; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21228444 - 10 Nov 2020

Cited by 8 | Viewed by 2862

Abstract

Metastasis is the main cause of cancer-related deaths. Anoikis is a type of apoptosis caused by cell detachment, and cancer cells become anoikis resistant such that they survive during circulation and can successfully metastasize. Therefore, sensitization of cancer cells to anoikis could prevent metastasis. Here, by screening for anoikis sensitizer using natural compounds, we found that pygenic acid A (PA), a natural compound from Prunella vulgaris, not only induced apoptosis but also sensitized the metastatic triple-negative breast cancer cell lines, MDA-MB-231 cells (human) and 4T1 cells (mouse), to anoikis. Apoptosis protein array and immunoblotting analysis revealed that PA downregulated the pro-survival proteins, including cIAP1, cIAP2, and survivin, leading to cell death of both attached and suspended cells. Interestingly, PA decreased the levels of proteins associated with anoikis resistance, including p21, cyclin D1, p-STAT3, and HO-1. Ectopic expression of active STAT3 attenuated PA-induced anoikis sensitivity. Although PA activated ER stress and autophagy, as determined by increases in the levels of characteristic markers, such as IRE1α, p-elF2α, LC3B I, and LC3B II, PA treatment resulted in p62 accumulation, which could be due to PA-induced defects in autophagy flux. PA also decreased metastatic characteristics, such as cell invasion, migration, wound closure, and 3D growth. Finally, lung metastasis of luciferase-labeled 4T1 cells decreased following PA treatment in a syngeneic mouse model when compared with the control. These data suggest that PA sensitizes metastatic breast cancer cells to anoikis via multiple pathways, such as inhibition of pro-survival pathways and activation of ER stress and autophagy, leading to the inhibition of metastasis. These findings suggest that sensitization to anoikis by PA could be used as a new therapeutic strategy to control the metastasis of breast cancer. Full article

(This article belongs to the Special Issue Cell Death in Biology and Diseases)

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16 pages, 2861 KiB

Open AccessArticle

Vernonia calvoana Shows Promise towards the Treatment of Ovarian Cancer

by Ariane T. Mbemi, Jennifer N. Sims, Clement G. Yedjou, Felicite K. Noubissi, Christian R. Gomez and Paul B. Tchounwou

Int. J. Mol. Sci. 2020, 21(12), 4429; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21124429 - 22 Jun 2020

Cited by 3 | Viewed by 3837

Abstract

The treatment for ovarian cancers includes chemotherapies which use drugs such as cisplatin, paclitaxel, carboplatin, platinum, taxanes, or their combination, and other molecular target therapies. However, these current therapies are often accompanied with side effects. Vernonia calvoana (VC) is a valuable edible medicinal plant that is widespread in West Africa. In vitro data in our lab demonstrated that VC crude extract inhibits human ovarian cancer cells in a dose-dependent manner, suggesting its antitumor activity. From the VC crude extract, we have generated 10 fractions and VC fraction 7 (F7) appears to show the highest antitumor activity towards ovarian cancer cells. However, the mechanisms by which VC F7 exerts its antitumor activity in cancer cells remain largely unknown. We hypothesized that VC F7 inhibits cell proliferation and induces DNA damage and cell cycle arrest in ovarian cells through oxidative stress. To test our hypothesis, we extracted and fractionated VC leaves. The effects of VC F7 were tested in OVCAR-3 cells. Viability was assessed by the means of MTS assay. Cell morphology was analyzed by acridine orange and propidium iodide (AO/PI) dye using a fluorescent microscope. Oxidative stress biomarkers were evaluated by the means of lipid peroxidation, catalase, and glutathione peroxidase assays, respectively. The degree of DNA damage was assessed by comet assay. Cell cycle distribution was assessed by flow cytometry. Data generated from the MTS assay demonstrated that VC F7 inhibits the growth of OVCAR-3 cells in a dose-dependent manner, showing a gradual increase in the loss of viability in VC F7-treated cells. Data obtained from the AO/PI dye assessment revealed morphological alterations and exhibited characteristics such as loss of cellular membrane integrity, cell shrinkage, cell membrane damage, organelle breakdown, and detachment from the culture plate. We observed a significant increase (p < 0.05) in the levels of malondialdhyde (MDA) production in treated cells compared to the control. A gradual decrease in both catalase and glutathione peroxidase activities were observed in the treated cells compared to the control. Data obtained from the comet assay showed a significant increase (p < 0.05) in the percentages of DNA cleavage and comet tail length. The results of the flow cytometry analysis indicated VC F7 treatment caused cell cycle arrest at the S-phase checkpoint. Taken together, our results demonstrate that VC F7 exerts its anticancer activity by inhibiting cell proliferation, inducing DNA damage, and causing cell cycle arrest through oxidative stress in OVAR-3 cells. This finding suggests that VC F7 may be a potential alternative dietary agent for the prevention and/or treatment of ovarian cancer. Full article

(This article belongs to the Special Issue Cell Death in Biology and Diseases)

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22 pages, 4505 KiB

Open AccessArticle

OsJAZ13 Negatively Regulates Jasmonate Signaling and Activates Hypersensitive Cell Death Response in Rice

by Xiujing Feng, Lei Zhang, Xiaoli Wei, Yun Zhou, Yan Dai and Zhen Zhu

Int. J. Mol. Sci. 2020, 21(12), 4379; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21124379 - 19 Jun 2020

Cited by 15 | Viewed by 3169

Abstract

Jasmonate ZIM-domain (JAZ) proteins belong to the subgroup of TIFY family and act as key regulators of jasmonate (JA) responses in plants. To date, only a few JAZ proteins have been characterized in rice. Here, we report the identification and function of rice OsJAZ13 gene. The gene encodes three different splice variants: OsJAZ13a, OsJAZ13b, and OsJAZ13c. The expression of OsJAZ13 was mainly activated in vegetative tissues and transiently responded to JA and ethylene. Subcellular localization analysis indicated OsJAZ13a is a nuclear protein. Yeast two-hybrid assays revealed OsJAZ13a directly interacts with OsMYC2, and also with OsCOI1, in a COR-dependent manner. Furthermore, OsJAZ13a recruited a general co-repressor OsTPL via an adaptor protein OsNINJA. Remarkably, overexpression of OsJAZ13a resulted in the attenuation of root by methyl JA. Furthermore, OsJAZ13a-overexpressing plants developed lesion mimics in the sheath after approximately 30–45 days of growth. Tillers with necrosis died a few days later. Gene-expression analysis suggested the role of OsJAZ13 in modulating the expression of JA/ethylene response-related genes to regulate growth and activate hypersensitive cell death. Taken together, these observations describe a novel regulatory mechanism in rice and provide the basis for elucidating the function of OsJAZ13 in signal transduction and cell death in plants. Full article

(This article belongs to the Special Issue Cell Death in Biology and Diseases)

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Review

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47 pages, 2655 KiB

Open AccessReview

Cell Death in Liver Diseases: A Review

by Layla Shojaie, Andrea Iorga and Lily Dara

Int. J. Mol. Sci. 2020, 21(24), 9682; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21249682 - 18 Dec 2020

Cited by 153 | Viewed by 11314

Abstract

Regulated cell death (RCD) is pivotal in directing the severity and outcome of liver injury. Hepatocyte cell death is a critical event in the progression of liver disease due to resultant inflammation leading to fibrosis. Apoptosis, necrosis, necroptosis, autophagy, and recently, pyroptosis and ferroptosis, have all been investigated in the pathogenesis of various liver diseases. These cell death subroutines display distinct features, while sharing many similar characteristics with considerable overlap and crosstalk. Multiple types of cell death modes can likely coexist, and the death of different liver cell populations may contribute to liver injury in each type of disease. This review addresses the known signaling cascades in each cell death pathway and its implications in liver disease. In this review, we describe the common findings in each disease model, as well as the controversies and the limitations of current data with a particular focus on cell death-related research in humans and in rodent models of alcoholic liver disease, non-alcoholic fatty liver disease and steatohepatitis (NASH/NAFLD), acetaminophen (APAP)-induced hepatotoxicity, autoimmune hepatitis, cholestatic liver disease, and viral hepatitis. Full article

(This article belongs to the Special Issue Cell Death in Biology and Diseases)

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32 pages, 3382 KiB

Open AccessReview

Influence of Microgravity on Apoptosis in Cells, Tissues, and Other Systems In Vivo and In Vitro

by Binod Prasad, Daniela Grimm, Sebastian M. Strauch, Gilmar Sidnei Erzinger, Thomas J. Corydon, Michael Lebert, Nils E. Magnusson, Manfred Infanger, Peter Richter and Marcus Krüger

Int. J. Mol. Sci. 2020, 21(24), 9373; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21249373 - 09 Dec 2020

Cited by 51 | Viewed by 6696

Abstract

All life forms have evolved under the constant force of gravity on Earth and developed ways to counterbalance acceleration load. In space, shear forces, buoyance-driven convection, and hydrostatic pressure are nullified or strongly reduced. When subjected to microgravity in space, the equilibrium between cell architecture and the external force is disturbed, resulting in changes at the cellular and sub-cellular levels (e.g., cytoskeleton, signal transduction, membrane permeability, etc.). Cosmic radiation also poses great health risks to astronauts because it has high linear energy transfer values that evoke complex DNA and other cellular damage. Space environmental conditions have been shown to influence apoptosis in various cell types. Apoptosis has important functions in morphogenesis, organ development, and wound healing. This review provides an overview of microgravity research platforms and apoptosis. The sections summarize the current knowledge of the impact of microgravity and cosmic radiation on cells with respect to apoptosis. Apoptosis-related microgravity experiments conducted with different mammalian model systems are presented. Recent findings in cells of the immune system, cardiovascular system, brain, eyes, cartilage, bone, gastrointestinal tract, liver, and pancreas, as well as cancer cells investigated under real and simulated microgravity conditions, are discussed. This comprehensive review indicates the potential of the space environment in biomedical research. Full article

(This article belongs to the Special Issue Cell Death in Biology and Diseases)

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27 pages, 2044 KiB

Open AccessReview

Antimicrobial Photoinactivation Approach Based on Natural Agents for Control of Bacteria Biofilms in Spacecraft

by Irina Buchovec, Alisa Gricajeva, Lilija Kalėdienė and Pranciškus Vitta

Int. J. Mol. Sci. 2020, 21(18), 6932; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186932 - 21 Sep 2020

Cited by 17 | Viewed by 4202

Abstract

A spacecraft is a confined system that is inhabited by a changing microbial consortium, mostly originating from life-supporting devices, equipment collected in pre-flight conditions, and crewmembers. Continuous monitoring of the spacecraft’s bioburden employing culture-based and molecular methods has shown the prevalence of various taxa, with human skin-associated microorganisms making a substantial contribution to the spacecraft microbiome. Microorganisms in spacecraft can prosper not only in planktonic growth mode but can also form more resilient biofilms that pose a higher risk to crewmembers’ health and the material integrity of the spacecraft’s equipment. Moreover, bacterial biofilms in space conditions are characterized by faster formation and acquisition of resistance to chemical and physical effects than under the same conditions on Earth, making most decontamination methods unsafe. There is currently no reported method available to combat biofilm formation in space effectively and safely. However, antibacterial photodynamic inactivation based on natural photosensitizers, which is reviewed in this work, seems to be a promising method. Full article

(This article belongs to the Special Issue Cell Death in Biology and Diseases)

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15 pages, 763 KiB

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Biological Functions and Therapeutic Potential of Lipocalin 2 in Cancer

by Ginette S. Santiago-Sánchez, Valentina Pita-Grisanti, Blanca Quiñones-Díaz, Kristyn Gumpper, Zobeida Cruz-Monserrate and Pablo E. Vivas-Mejía

Int. J. Mol. Sci. 2020, 21(12), 4365; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21124365 - 19 Jun 2020

Cited by 81 | Viewed by 8518

Abstract

Lipocalin-2 (LCN2) is a secreted glycoprotein linked to several physiological roles, including transporting hydrophobic ligands across cell membranes, modulating immune responses, maintaining iron homeostasis, and promoting epithelial cell differentiation. Although LNC2 is expressed at low levels in most human tissues, it is abundant in aggressive subtypes of cancer, including breast, pancreas, thyroid, ovarian, colon, and bile duct cancers. High levels of LCN2 have been associated with increased cell proliferation, angiogenesis, cell invasion, and metastasis. Moreover, LCN2 modulates the degradation, allosteric events, and enzymatic activity of matrix metalloprotease-9, a metalloprotease that promotes tumor cell invasion and metastasis. Hence, LCN2 has emerged as a potential therapeutic target against many cancer types. This review summarizes the most relevant findings regarding the expression, biological roles, and regulation of LCN2, as well as the proteins LCN2 interacts with in cancer. We also discuss the approaches to targeting LCN2 for cancer treatment that are currently under investigation, including the use of interference RNAs, antibodies, and gene editing. Full article

(This article belongs to the Special Issue Cell Death in Biology and Diseases)

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