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Article: The Role of NCOA4-Mediated Ferritinophagy in Ferroptosis.

Santana-Codina, Naiara / Gikandi, Ajami / Mancias, Joseph D

Advances in experimental medicine and biology

2021 Volume 1301, Page(s) 41–57

Abstract: Nuclear receptor coactivator 4 (NCOA4) is a selective cargo receptor that mediates the autophagic degradation of ferritin, the cytosolic iron storage complex, in a process known as ferritinophagy. NCOA4-mediated ferritinophagy is required to maintain ... ...

Abstract	Nuclear receptor coactivator 4 (NCOA4) is a selective cargo receptor that mediates the autophagic degradation of ferritin, the cytosolic iron storage complex, in a process known as ferritinophagy. NCOA4-mediated ferritinophagy is required to maintain intracellular and systemic iron homeostasis and thereby iron-dependent physiologic processes such as erythropoiesis. Given this role of ferritinophagy in regulating iron homeostasis, modulating NCOA4-mediated ferritinophagic flux alters sensitivity to ferroptosis, a non-apoptotic iron-dependent form of cell death triggered by peroxidation of polyunsaturated fatty acids (PUFAs). A role for ferroptosis has been established in the pathophysiology of cancer and neurodegeneration; however, the importance of ferritinophagy in these pathologies remains largely unknown. Here, we review the available evidence on biochemical regulation of NCOA4-mediated ferritinophagy and its role in modulating sensitivity to innate and induced ferroptosis in neurodegenerative diseases and cancer. Finally, we evaluate the potential of modulating ferritinophagy in combination with ferroptosis inducers as a therapeutic strategy.
MeSH term(s)	Autophagy ; Ferritins/genetics ; Ferroptosis ; Humans ; Iron/metabolism ; Nuclear Receptor Coactivators/genetics ; Nuclear Receptor Coactivators/metabolism
Chemical Substances	NCOA4 protein, human ; Nuclear Receptor Coactivators ; Ferritins (9007-73-2) ; Iron (E1UOL152H7)
Language	English
Publishing date	2021-08-16
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-3-030-62026-4_4
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Multicancer Early Detection Technologies: A Review Informed by Past Cancer Screening Studies.

Raoof, Sana / Lee, Richard J / Jajoo, Kunal / Mancias, Joseph D / Rebbeck, Timothy R / Skates, Steven J

Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology

2022 Volume 31, Issue 6, Page(s) 1139–1145

Abstract: More than 75% of cancer-related deaths occur from cancers for which we do not screen. New screening liquid biopsies may help fill these clinical gaps, although evidence of benefit still needs to be assessed. Which lessons can we learn from previous ... ...

Abstract	More than 75% of cancer-related deaths occur from cancers for which we do not screen. New screening liquid biopsies may help fill these clinical gaps, although evidence of benefit still needs to be assessed. Which lessons can we learn from previous efforts to guide those of the future? Screening trials for ovarian, prostate, pancreatic, and esophageal cancers are revisited to assess the evidence, which has been limited by small effect sizes, short duration of early-stage disease relative to screening frequency, study design, and confounding factors. Randomized controlled trials (RCT) to show mortality reduction have required millions of screening-years, two-decade durations, and been susceptible to external confounding. Future RCTs with late-stage incidence as a surrogate endpoint could substantially reduce these challenges, and clinical studies demonstrating safety and effectiveness of screening in high-risk populations may enable extrapolation to broader average-risk populations. Multicancer early detection tests provide an opportunity to advance these practical study designs. Conditional approvals based on RCTs with surrogate endpoints, contingent upon real world evidence generation and continuation of trials to definitive endpoints, may lower practical barriers to innovation in cancer screening and enable greater progress.
MeSH term(s)	Early Detection of Cancer ; Humans ; Incidence ; Male ; Mass Screening ; Neoplasms/diagnosis ; Neoplasms/prevention & control ; Prostate
Language	English
Publishing date	2022-03-19
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1153420-5
ISSN	1538-7755 ; 1055-9965
ISSN (online)	1538-7755
ISSN	1055-9965
DOI	10.1158/1055-9965.EPI-21-1443
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Article ; Online: Autophagy supports mitochondrial metabolism through the regulation of iron homeostasis in pancreatic cancer.

Mukhopadhyay, Subhadip / Encarnación-Rosado, Joel / Lin, Elaine Y / Sohn, Albert S W / Zhang, Huan / Mancias, Joseph D / Kimmelman, Alec C

Science advances

2023 Volume 9, Issue 16, Page(s) eadf9284

Abstract: Pancreatic ductal adenocarcinoma (PDAC) cells maintain a high level of autophagy, allowing them to thrive in an austere microenvironment. However, the processes through which autophagy promotes PDAC growth and survival are still not fully understood. ... ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) cells maintain a high level of autophagy, allowing them to thrive in an austere microenvironment. However, the processes through which autophagy promotes PDAC growth and survival are still not fully understood. Here, we show that autophagy inhibition in PDAC alters mitochondrial function by losing succinate dehydrogenase complex iron sulfur subunit B expression by limiting the availability of the labile iron pool. PDAC uses autophagy to maintain iron homeostasis, while other tumor types assessed require macropinocytosis, with autophagy being dispensable. We observed that cancer-associated fibroblasts can provide bioavailable iron to PDAC cells, promoting resistance to autophagy ablation. To overcome this cross-talk, we used a low-iron diet and demonstrated that this augmented the response to autophagy inhibition therapy in PDAC-bearing mice. Our work highlights a critical link between autophagy, iron metabolism, and mitochondrial function that may have implications for PDAC progression.
MeSH term(s)	Animals ; Mice ; Cell Line, Tumor ; Pancreatic Neoplasms/pathology ; Carcinoma, Pancreatic Ductal/metabolism ; Autophagy ; Homeostasis ; Mitochondria/metabolism ; Tumor Microenvironment ; Pancreatic Neoplasms
Language	English
Publishing date	2023-04-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.adf9284
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Article ; Online: PTEN-induced kinase PINK1 supports colorectal cancer growth by regulating the labile iron pool.

Chen, Brandon / Das, Nupur K / Talukder, Indrani / Singhal, Rashi / Castillo, Cristina / Andren, Anthony / Mancias, Joseph D / Lyssiotis, Costas A / Shah, Yatrik M

The Journal of biological chemistry

2023 Volume 299, Issue 5, Page(s) 104691

Abstract: Mitophagy is a cargo-specific autophagic process that recycles damaged mitochondria to promote mitochondrial turnover. PTEN-induced putative kinase 1 (PINK1) mediates the canonical mitophagic pathway. However, the role of PINK1 in diseases where ... ...

Abstract	Mitophagy is a cargo-specific autophagic process that recycles damaged mitochondria to promote mitochondrial turnover. PTEN-induced putative kinase 1 (PINK1) mediates the canonical mitophagic pathway. However, the role of PINK1 in diseases where mitophagy has been purported to play a role, such as colorectal cancer, is unclear. Our results here demonstrate that higher PINK1 expression is positively correlated with decreased colon cancer survival, and mitophagy is required for colon cancer growth. We show that doxycycline-inducible knockdown (KD) of PINK1 in a panel of colon cancer cell lines inhibited proliferation, whereas disruption of other mitophagy receptors did not impact cell growth. We observed that PINK KD led to a decrease in mitochondrial respiration, membrane hyperpolarization, accumulation of mitochondrial DNA, and depletion of antioxidant glutathione. In addition, mitochondria are important hubs for the utilization of iron and synthesizing iron-dependent cofactors such as heme and iron sulfur clusters. We observed an increase in the iron storage protein ferritin and a decreased labile iron pool in the PINK1 KD cells, but total cellular iron or markers of iron starvation/overload were not affected. Finally, cellular iron storage and the labile iron pool are maintained via autophagic degradation of ferritin (ferritinophagy). We found overexpressing nuclear receptor coactivator 4, a key adaptor for ferritinophagy, rescued cell growth and the labile iron pool in PINK1 KD cells. These results indicate that PINK1 integrates mitophagy and ferritinophagy to regulate intracellular iron availability and is essential for maintaining intracellular iron homeostasis to support survival and growth in colorectal cancer cells.
MeSH term(s)	Humans ; Colonic Neoplasms/genetics ; Colonic Neoplasms/pathology ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Ferritins ; Iron/metabolism ; Protein Kinases/genetics ; Protein Kinases/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Mitophagy
Chemical Substances	Ferritins (9007-73-2) ; Iron (E1UOL152H7) ; Protein Kinases (EC 2.7.-) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; PTEN-induced putative kinase (EC 2.7.11.1)
Language	English
Publishing date	2023-04-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2023.104691
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Article: NCOA4-Mediated Ferritinophagy: A Potential Link to Neurodegeneration.

Quiles Del Rey, Maria / Mancias, Joseph D

Frontiers in neuroscience

2019 Volume 13, Page(s) 238

Abstract: NCOA4 (Nuclear receptor coactivator 4) mediates the selective autophagic degradation of ferritin, the cellular cytosolic iron storage complex, thereby playing a critical role in intracellular and systemic iron homeostasis. Disruptions in iron homeostasis ...

Abstract	NCOA4 (Nuclear receptor coactivator 4) mediates the selective autophagic degradation of ferritin, the cellular cytosolic iron storage complex, thereby playing a critical role in intracellular and systemic iron homeostasis. Disruptions in iron homeostasis and autophagy are observed in several neurodegenerative disorders raising the possibility that NCOA4-mediated ferritinophagy links these two observations and may underlie, in part, the pathophysiology of neurodegeneration. Here, we review the available evidence detailing the molecular mechanisms of NCOA4-mediated ferritinophagy and recent studies examining its role in systemic iron homeostasis and erythropoiesis. We propose additional studies to examine the potential role of NCOA4 in the brain in the context of neurodegenerative diseases.
Language	English
Publishing date	2019-03-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2019.00238
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Article: The Role of Autophagy in Cancer.

Santana-Codina, Naiara / Mancias, Joseph D / Kimmelman, Alec C

Annual review of cancer biology

2019 Volume 1, Page(s) 19–39

Abstract: Autophagy is a highly conserved and regulated process that targets proteins and damaged organelles for lysosomal degradation to maintain cell metabolism, genomic integrity, and cell survival. The role of autophagy in cancer is dynamic and depends, in ... ...

Abstract	Autophagy is a highly conserved and regulated process that targets proteins and damaged organelles for lysosomal degradation to maintain cell metabolism, genomic integrity, and cell survival. The role of autophagy in cancer is dynamic and depends, in part, on tumor type and stage. Although autophagy constrains tumor initiation in normal tissue, some tumors rely on autophagy for tumor promotion and maintenance. Studies in genetically engineered mouse models support the idea that autophagy can constrain tumor initiation by regulating DNA damage and oxidative stress. In established tumors, autophagy can also be required for tumor maintenance, allowing tumors to survive environmental stress and providing intermediates for cell metabolism. Autophagy can also be induced in response to chemotherapeutics, acting as a drug-resistance mechanism. Therefore, targeting autophagy is an attractive cancer therapeutic option currently undergoing validation in clinical trials.
Language	English
Publishing date	2019-05-09
Publishing country	United States
Document type	Journal Article
ISSN	2472-3428
ISSN	2472-3428
DOI	10.1146/annurev-cancerbio-041816-122338
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Article ; Online: Endothelial ZIP8 plays a minor role in BMP6 regulation by iron in mice.

Fisher, Allison L / Phillips, Sydney / Wang, Chia-Yu / Paulo, Joao A / Xiao, Xia / Moschetta, Gillian A / Sridhar, Adhvaith / Mancias, Joseph D / Babitt, Jodie L

Blood

2024

Abstract: Iron-mediated induction of BMP6 expression by liver endothelial cells is essential for iron homeostasis regulation. We utilized multiple dietary and genetic mouse cohorts to demonstrate a minor functional role for ZIP8 in regulating BMP6 expression under ...

Abstract	Iron-mediated induction of BMP6 expression by liver endothelial cells is essential for iron homeostasis regulation. We utilized multiple dietary and genetic mouse cohorts to demonstrate a minor functional role for ZIP8 in regulating BMP6 expression under high-iron conditions.
Language	English
Publishing date	2024-03-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2023023385
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Article ; Online: Mechanisms of Selective Autophagy in Normal Physiology and Cancer.

Mancias, Joseph D / Kimmelman, Alec C

Journal of molecular biology

2016 Volume 428, Issue 9 Pt A, Page(s) 1659–1680

Abstract: Selective autophagy is critical for regulating cellular homeostasis by mediating lysosomal turnover of a wide variety of substrates including proteins, aggregates, organelles, and pathogens via a growing class of molecules termed selective autophagy ... ...

Abstract	Selective autophagy is critical for regulating cellular homeostasis by mediating lysosomal turnover of a wide variety of substrates including proteins, aggregates, organelles, and pathogens via a growing class of molecules termed selective autophagy receptors. The molecular mechanisms of selective autophagy receptor action and regulation are complex. Selective autophagy receptors link their bound cargo to the autophagosomal membrane by interacting with lipidated ATG8 proteins (LC3/GABARAP) that are intimately associated with the autophagosome membrane. The cargo signals that selective autophagy receptors recognize are diverse but their recognition can be broadly grouped into two classes, ubiquitin-dependent cargo recognition versus ubiquitin-independent. The roles of post-translational modification of selective autophagy receptors in regulating these pathways in response to stimuli are an active area of research. Here we will review recent advances in the identification of selective autophagy receptors and their regulatory mechanisms. Given its importance in maintaining cellular homeostasis, disruption of autophagy can lead to disease including neurodegeneration and cancer. The role of autophagy in cancer is complex as autophagy can mediate promotion or inhibition of tumorigenesis. Here we will also review the importance of autophagy in cancer with a specific focus on the role of selective autophagy receptors.
MeSH term(s)	Animals ; Autophagosomes/metabolism ; Autophagy ; Gene Expression Regulation ; Humans ; Neoplasms/physiopathology ; Signal Transduction ; Stress, Physiological
Language	English
Publishing date	2016-03-04
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80229-3
ISSN	1089-8638 ; 0022-2836
ISSN (online)	1089-8638
ISSN	0022-2836
DOI	10.1016/j.jmb.2016.02.027
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Article: The Role of NCOA4-Mediated Ferritinophagy in Health and Disease.

Santana-Codina, Naiara / Mancias, Joseph D

Pharmaceuticals (Basel, Switzerland)

2018 Volume 11, Issue 4

Abstract: Nuclear receptor coactivator 4 (NCOA4) is a selective cargo receptor that mediates the autophagic degradation of ferritin ("ferritinophagy"), the cytosolic iron storage complex. NCOA4-mediated ferritinophagy maintains intracellular iron homeostasis by ... ...

Abstract	Nuclear receptor coactivator 4 (NCOA4) is a selective cargo receptor that mediates the autophagic degradation of ferritin ("ferritinophagy"), the cytosolic iron storage complex. NCOA4-mediated ferritinophagy maintains intracellular iron homeostasis by facilitating ferritin iron storage or release according to demand. Ferritinophagy is involved in iron-dependent physiological processes such as erythropoiesis, where NCOA4 mediates ferritin iron release for mitochondrial heme synthesis. Recently, ferritinophagy has been shown to regulate ferroptosis, a newly described form of iron-dependent cell death mediated by excess lipid peroxidation. Dysregulation of iron metabolism and ferroptosis have been described in neurodegeneration, cancer, and infection, but little is known about the role of ferritinophagy in the pathogenesis of these diseases. Here, we will review the biochemical regulation of NCOA4, its contribution to physiological processes and its role in disease. Finally, we will discuss the potential of activating or inhibiting ferritinophagy and ferroptosis for therapeutic purposes.
Language	English
Publishing date	2018-10-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2193542-7
ISSN	1424-8247
ISSN	1424-8247
DOI	10.3390/ph11040114
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Article ; Online: Quantitative proteomics and RNA-sequencing of mouse liver endothelial cells identify novel regulators of BMP6 by iron.

Fisher, Allison L / Wang, Chia-Yu / Xu, Yang / Phillips, Sydney / Paulo, Joao A / Małachowska, Beata / Xiao, Xia / Fendler, Wojciech / Mancias, Joseph D / Babitt, Jodie L

iScience

2023 Volume 26, Issue 12, Page(s) 108555

Abstract: Hepcidin is the master hormone governing systemic iron homeostasis. Iron regulates hepcidin by activating bone morphogenetic protein (BMP)6 expression in liver endothelial cells (LECs), but the mechanisms are incompletely understood. To address this, we ... ...

Abstract	Hepcidin is the master hormone governing systemic iron homeostasis. Iron regulates hepcidin by activating bone morphogenetic protein (BMP)6 expression in liver endothelial cells (LECs), but the mechanisms are incompletely understood. To address this, we performed proteomics and RNA-sequencing on LECs from iron-adequate and iron-loaded mice. Gene set enrichment analysis identified transcription factors activated by high iron, including Nrf-2, which was previously reported to contribute to BMP6 regulation, and c-Jun.
Language	English
Publishing date	2023-11-22
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.108555
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