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  1. Article ; Online: COVID-19 and Diabetes

    Ernestina M. De Francesco / Veronica Vella / Antonino Belfiore

    Frontiers in Endocrinology, Vol

    The Importance of Controlling RAGE

    2020  Volume 11

    Keywords COVID-19 ; diabetes ; RAGE (receptor for advanced glycation end products) ; HMGB-1 (high mobility group box 1) ; pneumonia ; coagulation disorders ; Diseases of the endocrine glands. Clinical endocrinology ; RC648-665 ; covid19
    Language English
    Publishing date 2020-07-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article: COVID-19 and Diabetes: The Importance of Controlling RAGE.

    De Francesco, Ernestina M / Vella, Veronica / Belfiore, Antonino

    Frontiers in endocrinology

    2020  Volume 11, Page(s) 526

    MeSH term(s) Anti-Inflammatory Agents/therapeutic use ; Betacoronavirus/drug effects ; Betacoronavirus/isolation & purification ; COVID-19 ; Coronavirus Infections/drug therapy ; Coronavirus Infections/epidemiology ; Coronavirus Infections/virology ; Diabetes Complications/epidemiology ; Diabetes Complications/mortality ; Diabetes Complications/virology ; Diabetes Mellitus/metabolism ; Diabetes Mellitus/physiopathology ; Diabetes Mellitus/virology ; Humans ; Inflammation/drug therapy ; Inflammation/etiology ; Inflammation/metabolism ; Pandemics ; Pneumonia, Viral/drug therapy ; Pneumonia, Viral/epidemiology ; Pneumonia, Viral/virology ; Prognosis ; Receptor for Advanced Glycation End Products/antagonists & inhibitors ; Receptor for Advanced Glycation End Products/metabolism ; Risk Factors ; SARS-CoV-2 ; Survival Rate ; Virus Internalization/drug effects
    Chemical Substances Anti-Inflammatory Agents ; Receptor for Advanced Glycation End Products
    Keywords covid19
    Language English
    Publishing date 2020-07-14
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2020.00526
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: COVID-19 and Diabetes

    De Francesco, Ernestina M. / Vella, Veronica / Belfiore, Antonino

    Frontiers in Endocrinology

    The Importance of Controlling RAGE

    2020  Volume 11

    Keywords covid19
    Publisher Frontiers Media SA
    Publishing country ch
    Document type Article ; Online
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2020.00526
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Cancer stem cells (CSCs): metabolic strategies for their identification and eradication.

    De Francesco, Ernestina M / Sotgia, Federica / Lisanti, Michael P

    The Biochemical journal

    2018  Volume 475, Issue 9, Page(s) 1611–1634

    Abstract: Phenotypic and functional heterogeneity is one of the most relevant features of cancer cells within different tumor types and is responsible for treatment failure. Cancer stem cells (CSCs) are a population of cells with stem cell-like properties that are ...

    Abstract Phenotypic and functional heterogeneity is one of the most relevant features of cancer cells within different tumor types and is responsible for treatment failure. Cancer stem cells (CSCs) are a population of cells with stem cell-like properties that are considered to be the root cause of tumor heterogeneity, because of their ability to generate the full repertoire of cancer cell types. Moreover, CSCs have been invoked as the main drivers of metastatic dissemination and therapeutic resistance. As such, targeting CSCs may be a useful strategy to improve the effectiveness of classical anticancer therapies. Recently, metabolism has been considered as a relevant player in CSC biology, and indeed, oncogenic alterations trigger the metabolite-driven dissemination of CSCs. More interestingly, the action of metabolic pathways in CSC maintenance might not be merely a consequence of genomic alterations. Indeed, certain metabotypic phenotypes may play a causative role in maintaining the stem traits, acting as an orchestrator of stemness. Here, we review the current studies on the metabolic features of CSCs, focusing on the biochemical energy pathways involved in CSC maintenance and propagation. We provide a detailed overview of the plastic metabolic behavior of CSCs in response to microenvironment changes, genetic aberrations, and pharmacological stressors. In addition, we describe the potential of comprehensive metabolic approaches to identify and selectively eradicate CSCs, together with the possibility to 'force' CSCs within certain metabolic dependences, in order to effectively target such metabolic biochemical inflexibilities. Finally, we focus on targeting mitochondria to halt CSC dissemination and effectively eradicate cancer.
    MeSH term(s) Humans ; Metabolic Networks and Pathways ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/therapy ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Oxidative Phosphorylation ; Tumor Microenvironment
    Language English
    Publishing date 2018-05-09
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2969-5
    ISSN 1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
    ISSN (online) 1470-8728
    ISSN 0006-2936 ; 0306-3275 ; 0264-6021
    DOI 10.1042/BCJ20170164
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.110: 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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  6. Article ; Online: Crosstalk between Notch, HIF-1α and GPER in Breast Cancer EMT.

    De Francesco, Ernestina M / Maggiolini, Marcello / Musti, Anna Maria

    International journal of molecular sciences

    2018  Volume 19, Issue 7

    Abstract: The Notch signaling pathway acts in both physiological and pathological conditions, including embryonic development and tumorigenesis. In cancer progression, diverse mechanisms are involved in Notch-mediated biological responses, including angiogenesis ... ...

    Abstract The Notch signaling pathway acts in both physiological and pathological conditions, including embryonic development and tumorigenesis. In cancer progression, diverse mechanisms are involved in Notch-mediated biological responses, including angiogenesis and epithelial-mesenchymal-transition (EMT). During EMT, the activation of cellular programs facilitated by transcriptional repressors results in epithelial cells losing their differentiated features, like cell–cell adhesion and apical–basal polarity, whereas they gain motility. As it concerns cancer epithelial cells, EMT may be consequent to the evolution of genetic/epigenetic instability, or triggered by factors that can act within the tumor microenvironment. Following a description of the Notch signaling pathway and its major regulatory nodes, we focus on studies that have given insights into the functional interaction between Notch signaling and either hypoxia or estrogen in breast cancer cells, with a particular focus on EMT. Furthermore, we describe the role of hypoxia signaling in breast cancer cells and discuss recent evidence regarding a functional interaction between HIF-1α and GPER in both breast cancer cells and cancer-associated fibroblasts (CAFs). On the basis of these studies, we propose that a functional network between HIF-1α, GPER and Notch may integrate tumor microenvironmental cues to induce robust EMT in cancer cells. Further investigations are required in order to better understand how hypoxia and estrogen signaling may converge on Notch-mediated EMT within the context of the stroma and tumor cells interaction. However, the data discussed here may anticipate the potential benefits of further pharmacological strategies targeting breast cancer progression.
    MeSH term(s) Breast Neoplasms/metabolism ; Cell Line, Tumor ; Disease Progression ; Epithelial-Mesenchymal Transition ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Receptor Cross-Talk ; Receptors, Estrogen/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Receptors, Notch/metabolism ; Signal Transduction
    Chemical Substances GPER1 protein, human ; HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; Receptors, Estrogen ; Receptors, G-Protein-Coupled ; Receptors, Notch
    Language English
    Publishing date 2018-07-10
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms19072011
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  7. Article ; Online: Crosstalk between Notch, HIF-1α and GPER in Breast Cancer EMT

    Ernestina M. De Francesco / Marcello Maggiolini / Anna Maria Musti

    International Journal of Molecular Sciences, Vol 19, Iss 7, p

    2018  Volume 2011

    Abstract: The Notch signaling pathway acts in both physiological and pathological conditions, including embryonic development and tumorigenesis. In cancer progression, diverse mechanisms are involved in Notch-mediated biological responses, including angiogenesis ... ...

    Abstract The Notch signaling pathway acts in both physiological and pathological conditions, including embryonic development and tumorigenesis. In cancer progression, diverse mechanisms are involved in Notch-mediated biological responses, including angiogenesis and epithelial-mesenchymal-transition (EMT). During EMT, the activation of cellular programs facilitated by transcriptional repressors results in epithelial cells losing their differentiated features, like cell–cell adhesion and apical–basal polarity, whereas they gain motility. As it concerns cancer epithelial cells, EMT may be consequent to the evolution of genetic/epigenetic instability, or triggered by factors that can act within the tumor microenvironment. Following a description of the Notch signaling pathway and its major regulatory nodes, we focus on studies that have given insights into the functional interaction between Notch signaling and either hypoxia or estrogen in breast cancer cells, with a particular focus on EMT. Furthermore, we describe the role of hypoxia signaling in breast cancer cells and discuss recent evidence regarding a functional interaction between HIF-1α and GPER in both breast cancer cells and cancer-associated fibroblasts (CAFs). On the basis of these studies, we propose that a functional network between HIF-1α, GPER and Notch may integrate tumor microenvironmental cues to induce robust EMT in cancer cells. Further investigations are required in order to better understand how hypoxia and estrogen signaling may converge on Notch-mediated EMT within the context of the stroma and tumor cells interaction. However, the data discussed here may anticipate the potential benefits of further pharmacological strategies targeting breast cancer progression.
    Keywords notch signaling ; GPER ; estrogen ; hypoxia ; breast cancer ; EMT ; cancer associated fibroblast ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 610
    Language English
    Publishing date 2018-07-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: New insight into the catalytic -dependent and -independent roles of METTL3 in sustaining aberrant translation in chronic myeloid leukemia.

    Ianniello, Zaira / Sorci, Melissa / Ceci Ginistrelli, Lavinia / Iaiza, Alessia / Marchioni, Marcella / Tito, Claudia / Capuano, Ernestina / Masciarelli, Silvia / Ottone, Tiziana / Attrotto, Cristina / Rizzo, Manuela / Franceschini, Luca / de Pretis, Stefano / Voso, Maria Teresa / Pelizzola, Mattia / Fazi, Francesco / Fatica, Alessandro

    Cell death & disease

    2021  Volume 12, Issue 10, Page(s) 870

    Abstract: ... patients. Here, we reveal that the m ...

    Abstract Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm caused by the presence of tyrosine kinase BCR-ABL1 fusion protein, which deregulate transcription and mRNA translation. Tyrosine kinase inhibitors (TKIs) are the first-choice treatment. However, resistance to TKIs remains a challenge to cure CML patients. Here, we reveal that the m
    MeSH term(s) Adenosine/analogs & derivatives ; Adenosine/metabolism ; Catalysis ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cell Proliferation ; Cell Survival ; Drug Resistance, Neoplasm/drug effects ; Gene Knockdown Techniques ; Humans ; Imatinib Mesylate/pharmacology ; Imatinib Mesylate/therapeutic use ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/pathology ; Methyltransferases/metabolism ; Models, Biological ; Protein Biosynthesis ; Proto-Oncogene Proteins c-myc/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Up-Regulation
    Chemical Substances MYC protein, human ; PES1 protein, human ; Proto-Oncogene Proteins c-myc ; RNA, Messenger ; RNA-Binding Proteins ; Imatinib Mesylate (8A1O1M485B) ; N-methyladenosine (CLE6G00625) ; METTL14 protein, human (EC 2.1.1.-) ; Methyltransferases (EC 2.1.1.-) ; METTL3 protein, human (EC 2.1.1.62) ; Adenosine (K72T3FS567)
    Language English
    Publishing date 2021-09-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-021-04169-7
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  9. Article ; Online: G Protein-Coupled Receptors at the Crossroad between Physiologic and Pathologic Angiogenesis: Old Paradigms and Emerging Concepts.

    De Francesco, Ernestina M / Sotgia, Federica / Clarke, Robert B / Lisanti, Michael P / Maggiolini, Marcello

    International journal of molecular sciences

    2017  Volume 18, Issue 12

    Abstract: G protein-coupled receptors (GPCRs) have been implicated in transmitting signals across the extra- and intra-cellular compartments, thus allowing environmental stimuli to elicit critical biological responses. As GPCRs can be activated by an extensive ... ...

    Abstract G protein-coupled receptors (GPCRs) have been implicated in transmitting signals across the extra- and intra-cellular compartments, thus allowing environmental stimuli to elicit critical biological responses. As GPCRs can be activated by an extensive range of factors including hormones, neurotransmitters, phospholipids and other stimuli, their involvement in a plethora of physiological functions is not surprising. Aberrant GPCR signaling has been regarded as a major contributor to diverse pathologic conditions, such as inflammatory, cardiovascular and neoplastic diseases. In this regard, solid tumors have been demonstrated to activate an angiogenic program that relies on GPCR action to support cancer growth and metastatic dissemination. Therefore, the manipulation of aberrant GPCR signaling could represent a promising target in anticancer therapy. Here, we highlight the GPCR-mediated angiogenic function focusing on the molecular mechanisms and transduction effectors driving the patho-physiological vasculogenesis. Specifically, we describe evidence for the role of heptahelic receptors and associated G proteins in promoting angiogenic responses in pathologic conditions, especially tumor angiogenesis and progression. Likewise, we discuss opportunities to manipulate aberrant GPCR-mediated angiogenic signaling for therapeutic benefit using innovative GPCR-targeted and patient-tailored pharmacological strategies.
    MeSH term(s) Animals ; Disease Progression ; Humans ; Models, Biological ; Neoplasms/blood supply ; Neoplasms/metabolism ; Neoplasms/physiopathology ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/physiopathology ; Neovascularization, Physiologic/physiology ; Receptors, G-Protein-Coupled/metabolism ; Receptors, G-Protein-Coupled/physiology ; Signal Transduction
    Chemical Substances Receptors, G-Protein-Coupled
    Language English
    Publishing date 2017-12-14
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms18122713
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  10. Article ; Online: G Protein-Coupled Receptors at the Crossroad between Physiologic and Pathologic Angiogenesis

    Ernestina M. De Francesco / Federica Sotgia / Robert B. Clarke / Michael P. Lisanti / Marcello Maggiolini

    International Journal of Molecular Sciences, Vol 18, Iss 12, p

    Old Paradigms and Emerging Concepts

    2017  Volume 2713

    Abstract: G protein-coupled receptors (GPCRs) have been implicated in transmitting signals across the extra- and intra-cellular compartments, thus allowing environmental stimuli to elicit critical biological responses. As GPCRs can be activated by an extensive ... ...

    Abstract G protein-coupled receptors (GPCRs) have been implicated in transmitting signals across the extra- and intra-cellular compartments, thus allowing environmental stimuli to elicit critical biological responses. As GPCRs can be activated by an extensive range of factors including hormones, neurotransmitters, phospholipids and other stimuli, their involvement in a plethora of physiological functions is not surprising. Aberrant GPCR signaling has been regarded as a major contributor to diverse pathologic conditions, such as inflammatory, cardiovascular and neoplastic diseases. In this regard, solid tumors have been demonstrated to activate an angiogenic program that relies on GPCR action to support cancer growth and metastatic dissemination. Therefore, the manipulation of aberrant GPCR signaling could represent a promising target in anticancer therapy. Here, we highlight the GPCR-mediated angiogenic function focusing on the molecular mechanisms and transduction effectors driving the patho-physiological vasculogenesis. Specifically, we describe evidence for the role of heptahelic receptors and associated G proteins in promoting angiogenic responses in pathologic conditions, especially tumor angiogenesis and progression. Likewise, we discuss opportunities to manipulate aberrant GPCR-mediated angiogenic signaling for therapeutic benefit using innovative GPCR-targeted and patient-tailored pharmacological strategies.
    Keywords GPCR ; tumor angiogenesis ; tumor microenvironment ; VEGF ; HIF-1 ; GPER ; SDF-1 ; sphingosine-1P ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Language English
    Publishing date 2017-12-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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