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Article ; Online: The role of VEGF 165b in pathophysiology.

Peiris-Pagès, Maria

2012 Volume 6, Issue 6, Page(s) 561–568

Abstract: Anti-angiogenic vascular endothelial growth factor A (VEGF) 165b and pro-angiogenic VEGF 165 are generated from the same transcript, and their relative amounts are dependent on alternative splicing. The role of VEGF 165b has not been investigated in as ... ...

Abstract	Anti-angiogenic vascular endothelial growth factor A (VEGF) 165b and pro-angiogenic VEGF 165 are generated from the same transcript, and their relative amounts are dependent on alternative splicing. The role of VEGF 165b has not been investigated in as much detail as VEGF 165, although it appears to be highly expressed in non-angiogenic tissues and, in contrast with VEGF 165, is downregulated in tumors and other pathologies associated with abnormal neovascularization such as diabetic retinopathy or Denys Drash syndrome. VEGF 165b inhibits VEGFR2 signaling by inducing differential phosphorylation, and it can be used to block angiogenesis in in vivo models of tumorigenesis and angiogenesis-related eye disease. Recent reports have identified three serine/arginine-rich proteins, SRSF1, SRSF2 and SRSF6, and studied their role in regulating terminal splice-site selection. Since the balance of VEGF isoforms is lost in cancer and angiogenesis-related conditions, control of VEGF splicing could also be used as a basis for therapy in these diseases.
MeSH term(s)	Alternative Splicing ; Animals ; Capillary Permeability ; Denys-Drash Syndrome/metabolism ; Denys-Drash Syndrome/physiopathology ; Diabetic Retinopathy/metabolism ; Diabetic Retinopathy/physiopathology ; Glomerulonephritis/metabolism ; Glomerulonephritis/physiopathology ; Humans ; Neoplasms/metabolism ; Neoplasms/physiopathology ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/physiopathology ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Phosphorylation ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Serine-Arginine Splicing Factors ; Signal Transduction ; Vascular Endothelial Growth Factor A/genetics ; Vascular Endothelial Growth Factor A/metabolism ; Vascular Endothelial Growth Factor Receptor-2/metabolism
Chemical Substances	Nuclear Proteins ; Protein Isoforms ; RNA-Binding Proteins ; VEGFA protein, human ; Vascular Endothelial Growth Factor A ; Serine-Arginine Splicing Factors (170974-22-8) ; Vascular Endothelial Growth Factor Receptor-2 (EC 2.7.10.1)
Language	English
Publishing date	2012-10-17
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2268518-2
ISSN	1933-6926 ; 1933-6918
ISSN (online)	1933-6926
ISSN	1933-6918
DOI	10.4161/cam.22439
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Article ; Online: Mitochondrial and ribosomal biogenesis are new hallmarks of stemness, oncometabolism and biomass accumulation in cancer: Mito-stemness and ribo-stemness features.

Peiris-Pagès, Maria / Ozsvári, Béla / Sotgia, Federica / Lisanti, Michael P

Aging

2019 Volume 11, Issue 14, Page(s) 4801–4835

Abstract: Using proteomics analysis, we previously compared MCF7 breast cancer cells grown as 3D tumor spheres, with the same cell line grown as monolayers. Our results indicated that during 3D anchorage-independent growth, the cellular machinery associated with i) ...

Abstract	Using proteomics analysis, we previously compared MCF7 breast cancer cells grown as 3D tumor spheres, with the same cell line grown as monolayers. Our results indicated that during 3D anchorage-independent growth, the cellular machinery associated with i) mitochondrial biogenesis and ii) ribosomal biogenesis, were both significantly increased. Here, for simplicity, we refer to these two new oncogenic hallmarks as "mito-stemness" and "ribo-stemness" features. We have now applied this same type of strategy to begin to understand how fibroblasts and MCF7 breast cancer cells change their molecular phenotype, when they are co-cultured together. We have previously shown that MCF7-fibroblast co-cultures are a valuable model of resistance to apoptosis induced by hormonal therapies, such as Tamoxifen and Fulvestrant. Here, we directly show that these mixed co-cultures demonstrate the induction of mito-stemness and ribo-stemness features, likely reflecting a mechanism for cancer cells to increase their capacity for accumulating biomass. In accordance with the onset of a stem-like phenotype, KRT19 (keratin 19) was induced by ~6-fold during co-culture. KRT19 is a well-established epithelial CSC marker that is used clinically to identify metastatic breast cancer cells in sentinel lymph node biopsies. The potential molecular therapeutic targets that we identified by label-free proteomics of MCF7-fibroblast co-cultures were then independently validated using a bioinformatics approach. More specifically, we employed publically-available transcriptional profiling data derived from primary tumor samples from breast cancer patients, which were previously subjected to laser-capture micro-dissection, to physically separate breast cancer cells from adjacent tumor stroma. This allowed us to directly validate that the proteins up-regulated in this co-culture model were also transcriptionally elevated in patient-derived breast cancer cells
MeSH term(s)	Breast Neoplasms ; Cellular Reprogramming/physiology ; Coculture Techniques ; Drug Resistance, Neoplasm/physiology ; Female ; Fibroblasts/metabolism ; Humans ; MCF-7 Cells ; Mitochondria/metabolism ; Neoplastic Stem Cells/physiology ; Organelle Biogenesis ; Phenotype ; Proteomics ; Ribosomes/metabolism
Language	English
Publishing date	2019-07-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.102054
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Article ; Online: Mitochondrial fission as a driver of stemness in tumor cells: mDIVI1 inhibits mitochondrial function, cell migration and cancer stem cell (CSC) signalling.

Peiris-Pagès, Maria / Bonuccelli, Gloria / Sotgia, Federica / Lisanti, Michael P

Oncotarget

2018 Volume 9, Issue 17, Page(s) 13254–13275

Abstract: Mitochondria are dynamic organelles frequently undergoing fission and fusion events to maintain their integrity, bioenergetics and spatial distribution, which is fundamental to the processes of cell survival. Disruption in mitochondrial dynamics plays a ... ...

Abstract	Mitochondria are dynamic organelles frequently undergoing fission and fusion events to maintain their integrity, bioenergetics and spatial distribution, which is fundamental to the processes of cell survival. Disruption in mitochondrial dynamics plays a role in cancer. Therefore, proteins involved in regulating mitochondrial dynamics are potential targets for treatment. mDIVI1 is an inhibitor of the mitochondrial fission protein DRP1, which induces i) mitochondrial oxidative stress and ii) effectively reduces mitochondrial metabolism. We show here that mDIVI1 is able to inhibit 3D tumorsphere forming capacity, cell migration and stemness-related signalling in breast cancer cells, indicating that mDIVI1 can potentially be used for the therapeutic elimination of cancer stem cells (CSCs).
Language	English
Publishing date	2018-03-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.24285
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Article: Functional Characterisation of the ATOH1 Molecular Subtype Indicates a Pro-Metastatic Role in Small Cell Lung Cancer.

bioRxiv : the preprint server for biology

2024

Abstract: Molecular subtypes of Small Cell Lung Cancer (SCLC) have been described based on differential expression of transcription factors (TFs) ...

Abstract	Molecular subtypes of Small Cell Lung Cancer (SCLC) have been described based on differential expression of transcription factors (TFs)
Language	English
Publishing date	2024-02-17
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.02.16.580247
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Article: Doxycycline and therapeutic targeting of the DNA damage response in cancer cells: old drug, new purpose.

Peiris-Pagès, Maria / Sotgia, Federica / Lisanti, Michael P

Oncoscience

2015 Volume 2, Issue 8, Page(s) 696–699

Abstract: There is a small proportion of cells within a tumour with self-renewing properties, which is resistant to conventional therapy, and is responsible for tumour initiation, maintenance and metastasis. These cells are known as cancer stem cells (CSCs) or ... ...

Abstract	There is a small proportion of cells within a tumour with self-renewing properties, which is resistant to conventional therapy, and is responsible for tumour initiation, maintenance and metastasis. These cells are known as cancer stem cells (CSCs) or tumour-initiating cells (TICs) [1]. Recent publications identify several antibiotics, such as salinomycin or doxycycline, as selective CSCs inhibitors [2-4]. However, the mechanisms of action of these antibiotics on CSCs are not fully understood.
Language	English
Publishing date	2015-08-24
Publishing country	United States
Document type	Journal Article
ISSN	2331-4737
ISSN	2331-4737
DOI	10.18632/oncoscience.215
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Article ; Online: Chemotherapy induces the cancer-associated fibroblast phenotype, activating paracrine Hedgehog-GLI signalling in breast cancer cells.

Peiris-Pagès, Maria / Sotgia, Federica / Lisanti, Michael P

Oncotarget

2015 Volume 6, Issue 13, Page(s) 10728–10745

Abstract: Cancer cells recruit normal cells such as fibroblasts to establish reactive microenvironments. Via metabolic stress, catabolism and inflammation, these cancer-associated fibroblasts set up a synergistic relationship with tumour cells, that contributes to ...

Abstract	Cancer cells recruit normal cells such as fibroblasts to establish reactive microenvironments. Via metabolic stress, catabolism and inflammation, these cancer-associated fibroblasts set up a synergistic relationship with tumour cells, that contributes to their malignancy and resistance to therapy. Given that chemotherapy is a systemic treatment, the possibility that healthy cell damage affects the metastatic risk or the prospect of developing a second malignancy becomes relevant. Here, we demonstrate that standard chemotherapies phenotypically and metabolically transform stromal fibroblasts into cancer-associated fibroblasts, leading to the emergence of a highly glycolytic, autophagic and pro-inflammatory microenvironment. This catabolic microenvironment, in turn, activates stemness (Sonic hedgehog/GLI signalling), antioxidant response and interferon-mediated signalling, in adjacent breast cancer cells. Thus, we propose a model by which chemotherapy-induced catabolism in healthy fibroblasts constitutes a source of energy-rich nutrients and inflammatory cytokines that would activate stemness in adjacent epithelial cells, possibly triggering new tumorigenic processes. In this context, immune cell recruitment would be also stimulated to further support malignancy.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antioxidants/metabolism ; Autophagy/drug effects ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cellular Senescence/drug effects ; Coculture Techniques ; Cytokines/metabolism ; Dose-Response Relationship, Drug ; Female ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Glycolysis/drug effects ; Hedgehog Proteins/metabolism ; Humans ; Inflammation Mediators/metabolism ; MCF-7 Cells ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Oxidative Stress/drug effects ; Paracrine Communication/drug effects ; Phenotype ; Signal Transduction/drug effects ; Time Factors ; Transcription Factors/metabolism ; Transfection ; Tumor Microenvironment ; Zinc Finger Protein GLI1
Chemical Substances	Antineoplastic Agents ; Antioxidants ; Cytokines ; GLI1 protein, human ; Hedgehog Proteins ; Inflammation Mediators ; Transcription Factors ; Zinc Finger Protein GLI1
Language	English
Publishing date	2015-05-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.3828
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Article ; Online: Crosstalk between small-cell lung cancer cells and astrocytes mimics brain development to promote brain metastasis.

Nature cell biology

2023 Volume 25, Issue 10, Page(s) 1506–1519

Abstract: Brain metastases represent an important clinical problem for patients with small-cell lung cancer (SCLC). However, the mechanisms underlying SCLC growth in the brain remain poorly understood. Here, using intracranial injections in mice and assembloids ... ...

Abstract	Brain metastases represent an important clinical problem for patients with small-cell lung cancer (SCLC). However, the mechanisms underlying SCLC growth in the brain remain poorly understood. Here, using intracranial injections in mice and assembloids between SCLC aggregates and human cortical organoids in culture, we found that SCLC cells recruit reactive astrocytes to the tumour microenvironment. This crosstalk between SCLC cells and astrocytes drives the induction of gene expression programmes that are similar to those found during early brain development in neurons and astrocytes. Mechanistically, the brain development factor Reelin, secreted by SCLC cells, recruits astrocytes to brain metastases. These astrocytes in turn promote SCLC growth by secreting neuronal pro-survival factors such as SERPINE1. Thus, SCLC brain metastases grow by co-opting mechanisms involved in reciprocal neuron-astrocyte interactions during brain development. Targeting such developmental programmes activated in this cancer ecosystem may help prevent and treat brain metastases.
MeSH term(s)	Humans ; Animals ; Mice ; Astrocytes/pathology ; Lung Neoplasms/metabolism ; Ecosystem ; Brain Neoplasms/metabolism ; Brain/metabolism ; Tumor Microenvironment
Language	English
Publishing date	2023-10-02
Publishing country	England
Document type	Journal Article
ZDB-ID	1474722-4
ISSN	1476-4679 ; 1465-7392
ISSN (online)	1476-4679
ISSN	1465-7392
DOI	10.1038/s41556-023-01241-6
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Zs.A 5169: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Cancer metabolism: a therapeutic perspective.

Martinez-Outschoorn, Ubaldo E / Peiris-Pagés, Maria / Pestell, Richard G / Sotgia, Federica / Lisanti, Michael P

Nature reviews. Clinical oncology

2017 Volume 14, Issue 2, Page(s) 113

Language	English
Publishing date	2017-02
Publishing country	England
Document type	Journal Article
ZDB-ID	2491410-1
ISSN	1759-4782 ; 1759-4774
ISSN (online)	1759-4782
ISSN	1759-4774
DOI	10.1038/nrclinonc.2017.1
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Zs.A 6029: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Cancer metabolism: a therapeutic perspective.

Martinez-Outschoorn, Ubaldo E / Peiris-Pagés, Maria / Pestell, Richard G / Sotgia, Federica / Lisanti, Michael P

Nature reviews. Clinical oncology

2017 Volume 14, Issue 1, Page(s) 11–31

Abstract: Awareness that the metabolic phenotype of cells within tumours is heterogeneous - and distinct from that of their normal counterparts - is growing. In general, tumour cells metabolize glucose, lactate, pyruvate, hydroxybutyrate, acetate, glutamine, and ... ...

Abstract	Awareness that the metabolic phenotype of cells within tumours is heterogeneous - and distinct from that of their normal counterparts - is growing. In general, tumour cells metabolize glucose, lactate, pyruvate, hydroxybutyrate, acetate, glutamine, and fatty acids at much higher rates than their nontumour equivalents; however, the metabolic ecology of tumours is complex because they contain multiple metabolic compartments, which are linked by the transfer of these catabolites. This metabolic variability and flexibility enables tumour cells to generate ATP as an energy source, while maintaining the reduction-oxidation (redox) balance and committing resources to biosynthesis - processes that are essential for cell survival, growth, and proliferation. Importantly, experimental evidence indicates that metabolic coupling between cell populations with different, complementary metabolic profiles can induce cancer progression. Thus, targeting the metabolic differences between tumour and normal cells holds promise as a novel anticancer strategy. In this Review, we discuss how cancer cells reprogramme their metabolism and that of other cells within the tumour microenvironment in order to survive and propagate, thus driving disease progression; in particular, we highlight potential metabolic vulnerabilities that might be targeted therapeutically.
MeSH term(s)	Acetyl Coenzyme A/metabolism ; Adaptation, Physiological ; Amino Acids/metabolism ; Antineoplastic Agents/therapeutic use ; Antioxidants/metabolism ; Autophagy/physiology ; Blood Glucose/metabolism ; Energy Metabolism/drug effects ; Epigenomics ; Fatty Acids/metabolism ; Genetic Heterogeneity ; Glutamic Acid/metabolism ; Glutamine/metabolism ; Humans ; Ketone Bodies/metabolism ; Lactic Acid/metabolism ; Lipids/biosynthesis ; Mitochondria/drug effects ; Mitochondrial Ribosomes/drug effects ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Nucleic Acids/biosynthesis ; Oxidative Stress/drug effects ; Pyruvic Acid/metabolism ; TOR Serine-Threonine Kinases/antagonists & inhibitors ; Transcription Factors/metabolism ; Tumor Microenvironment
Chemical Substances	Amino Acids ; Antineoplastic Agents ; Antioxidants ; Blood Glucose ; Fatty Acids ; Ketone Bodies ; Lipids ; Nucleic Acids ; Transcription Factors ; Glutamine (0RH81L854J) ; Lactic Acid (33X04XA5AT) ; Glutamic Acid (3KX376GY7L) ; Acetyl Coenzyme A (72-89-9) ; Pyruvic Acid (8558G7RUTR) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1)
Language	English
Publishing date	2017-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2491410-1
ISSN	1759-4782 ; 1759-4774
ISSN (online)	1759-4782
ISSN	1759-4774
DOI	10.1038/nrclinonc.2016.60
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Article ; Online: Cancer stem cell metabolism.

Peiris-Pagès, Maria / Martinez-Outschoorn, Ubaldo E / Pestell, Richard G / Sotgia, Federica / Lisanti, Michael P

Breast cancer research : BCR

2016 Volume 18, Issue 1, Page(s) 55

Abstract: Cancer is now viewed as a stem cell disease. There is still no consensus on the metabolic characteristics of cancer stem cells, with several studies indicating that they are mainly glycolytic and others pointing instead to mitochondrial metabolism as ... ...

Abstract	Cancer is now viewed as a stem cell disease. There is still no consensus on the metabolic characteristics of cancer stem cells, with several studies indicating that they are mainly glycolytic and others pointing instead to mitochondrial metabolism as their principal source of energy. Cancer stem cells also seem to adapt their metabolism to microenvironmental changes by conveniently shifting energy production from one pathway to another, or by acquiring intermediate metabolic phenotypes. Determining the role of cancer stem cell metabolism in carcinogenesis has become a major focus in cancer research, and substantial efforts are conducted towards discovering clinical targets.
MeSH term(s)	Animals ; Energy Metabolism ; Female ; Humans ; Metabolic Networks and Pathways ; Mitochondria/metabolism ; Neoplasms/drug therapy ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/metabolism ; Tumor Microenvironment/immunology
Language	English
Publishing date	2016-05-24
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2015059-3
ISSN	1465-542X ; 1465-5411
ISSN (online)	1465-542X
ISSN	1465-5411
DOI	10.1186/s13058-016-0712-6
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