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  1. Article ; Online: Extracellular matrix guidance of autophagy: a mechanism regulating cancer growth.

    Chen, Carolyn G / Iozzo, Renato V

    Open biology

    2022  Volume 12, Issue 1, Page(s) 210304

    Abstract: The extracellular matrix (ECM) exists as a dynamic network of biophysical and biochemical factors that maintain tissue homeostasis. Given its sensitivity to changes in the intra- and extracellular space, the plasticity of the ECM can be pathological in ... ...

    Abstract The extracellular matrix (ECM) exists as a dynamic network of biophysical and biochemical factors that maintain tissue homeostasis. Given its sensitivity to changes in the intra- and extracellular space, the plasticity of the ECM can be pathological in driving disease through aberrant matrix remodelling. In particular, cancer uses the matrix for its proliferation, angiogenesis, cellular reprogramming and metastatic spread. An emerging field of matrix biology focuses on proteoglycans that regulate autophagy, an intracellular process that plays both critical and contextual roles in cancer. Here, we review the most prominent autophagic modulators from the matrix and the current understanding of the cellular pathways and signalling cascades that mechanistically drive their autophagic function. We then critically assess how their autophagic functions influence tumorigenesis, emphasizing the complexities and stage-dependent nature of this relationship in cancer. We highlight novel emerging data on immunoglobulin-containing and proline-rich receptor-1, heparanase and thrombospondin 1 in autophagy and cancer. Finally, we further discuss the pro- and anti-autophagic modulators originating from the ECM, as well as how these proteoglycans and other matrix constituents specifically influence cancer progression.
    MeSH term(s) Autophagy ; Extracellular Matrix/metabolism ; Humans ; Neoplasms/metabolism ; Neovascularization, Pathologic/metabolism ; Proteoglycans/metabolism
    Chemical Substances Proteoglycans
    Language English
    Publishing date 2022-01-05
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2630944-0
    ISSN 2046-2441 ; 2046-2441
    ISSN (online) 2046-2441
    ISSN 2046-2441
    DOI 10.1098/rsob.210304
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: The Role of Decorin Proteoglycan in Mitophagy.

    Neill, Thomas / Iozzo, Renato V

    Cancers

    2022  Volume 14, Issue 3

    Abstract: Proteoglycans are emerging as critical regulators of intracellular catabolism. This rise in prominence has transformed our basic understanding and alerted us to the existence of non-canonical pathways, independent of nutrient deprivation, that potently ... ...

    Abstract Proteoglycans are emerging as critical regulators of intracellular catabolism. This rise in prominence has transformed our basic understanding and alerted us to the existence of non-canonical pathways, independent of nutrient deprivation, that potently control the autophagy downstream of a cell surface receptor. As a member of the small leucine-rich proteoglycan gene family, decorin has single-handedly pioneered the connection between extracellular matrix signaling and autophagy regulation. Soluble decorin evokes protracted endothelial cell autophagy via Peg3 and breast carcinoma cell mitophagy via mitostatin by interacting with VEGFR2 or the MET receptor tyrosine kinase, respectively. In this paper, we give a mechanistic perspective of the vital factors underlying the nutrient-independent, SLRP-dependent programs utilized for autophagic and/or mitophagic progression in breast cancer. Future protein therapies based on decorin (or fellow proteoglycan members) will represent a quantum leap forward in transforming autophagic progression into a powerful tool to control intracellular cell catabolism from the outside.
    Language English
    Publishing date 2022-02-04
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers14030804
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  3. Book: Proteoglycan protocols

    Iozzo, Renato V.

    (Methods in molecular biology ; 171)

    2001  

    Author's details ed. by Renato V. Iozzo
    Series title Methods in molecular biology ; 171
    Collection
    Keywords Proteoglykane ; Methode ; Protoglykane ; Molekularbiologie
    Subject Methodik ; Verfahren ; Technik ; Methoden ; Molekulare Biologie ; Proteoglycane
    Language English
    Size XVI, 558 S. : Ill., graph. Darst.
    Publisher Humana Press
    Publishing place Totowa, NJ
    Publishing country United States
    Document type Book
    HBZ-ID HT013125289
    ISBN 0-89603-759-2 ; 978-0-89603-759-5
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2001 A 4661 order for loan Magazin

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  4. Article ; Online: Global impact of proteoglycan science on human diseases.

    Xie, Christopher / Schaefer, Liliana / Iozzo, Renato V

    iScience

    2023  Volume 26, Issue 11, Page(s) 108095

    Abstract: In this comprehensive review, we will dissect the impact of research on proteoglycans focusing on recent developments involved in their synthesis, degradation, and interactions, while critically assessing their usefulness in various biological processes. ...

    Abstract In this comprehensive review, we will dissect the impact of research on proteoglycans focusing on recent developments involved in their synthesis, degradation, and interactions, while critically assessing their usefulness in various biological processes. The emerging roles of proteoglycans in global infections, specifically the SARS-CoV-2 pandemic, and their rising functions in regenerative medicine and biomaterial science have significantly affected our current view of proteoglycans and related compounds. The roles of proteoglycans in cancer biology and their potential use as a next-generation protein-based adjuvant therapy to combat cancer is also emerging as a constructive and potentially beneficial therapeutic strategy. We will discuss the role of proteoglycans in selected and emerging areas of proteoglycan science, such as neurodegenerative diseases, autophagy, angiogenesis, cancer, infections and their impact on mammalian diseases.
    Language English
    Publishing date 2023-10-04
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2023.108095
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  5. Book: Proteoglycans

    Iozzo, Renato V.

    structure, biology, and molecular interactions

    2000  

    Author's details ed. by Renato V. Iozzo
    Language English
    Size IX, 422 S. : Ill., graph. Darst.
    Publisher Dekker
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT012749355
    ISBN 0-8247-0334-0 ; 978-0-8247-0334-9
    Database Catalogue ZB MED Medicine, Health

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  6. Article ; Online: Decorin suppresses tumor lymphangiogenesis: A mechanism to curtail cancer progression.

    Mondal, Dipon K / Xie, Christopher / Pascal, Gabriel J / Buraschi, Simone / Iozzo, Renato V

    Proceedings of the National Academy of Sciences of the United States of America

    2024  Volume 121, Issue 18, Page(s) e2317760121

    Abstract: The complex interplay between malignant cells and the cellular and molecular components of the tumor stroma is a key aspect of cancer growth and development. These tumor-host interactions are often affected by soluble bioactive molecules such as ... ...

    Abstract The complex interplay between malignant cells and the cellular and molecular components of the tumor stroma is a key aspect of cancer growth and development. These tumor-host interactions are often affected by soluble bioactive molecules such as proteoglycans. Decorin, an archetypical small leucine-rich proteoglycan primarily expressed by stromal cells, affects cancer growth in its soluble form by interacting with several receptor tyrosine kinases (RTK). Overall, decorin leads to a context-dependent and protracted cessation of oncogenic RTK activity by attenuating their ability to drive a prosurvival program and to sustain a proangiogenic network. Through an unbiased transcriptomic analysis using deep RNAseq, we identified that decorin down-regulated a cluster of tumor-associated genes involved in lymphatic vessel (LV) development when systemically delivered to mice harboring breast carcinoma allografts. We found that Lyve1 and Podoplanin, two established markers of LVs, were markedly suppressed at both the mRNA and protein levels, and this suppression correlated with a significant reduction in tumor LVs. We further identified that soluble decorin, but not its homologous proteoglycan biglycan, inhibited LV sprouting in an ex vivo 3D model of lymphangiogenesis. Mechanistically, we found that decorin interacted with vascular endothelial growth factor receptor 3 (VEGFR3), the main lymphatic RTK, and its activity was required for the decorin-mediated block of lymphangiogenesis. Finally, we identified that Lyve1 was in part degraded via decorin-evoked autophagy in a nutrient- and energy-independent manner. These findings implicate decorin as a biological factor with antilymphangiogenic activity and provide a potential therapeutic agent for curtailing breast cancer growth and metastasis.
    MeSH term(s) Decorin/metabolism ; Decorin/genetics ; Lymphangiogenesis ; Animals ; Mice ; Humans ; Female ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Breast Neoplasms/genetics ; Lymphatic Vessels/metabolism ; Lymphatic Vessels/pathology ; Cell Line, Tumor ; Disease Progression ; Vesicular Transport Proteins/metabolism ; Vesicular Transport Proteins/genetics ; Membrane Glycoproteins/metabolism ; Membrane Glycoproteins/genetics ; Gene Expression Regulation, Neoplastic
    Chemical Substances Decorin ; Vesicular Transport Proteins ; Membrane Glycoproteins ; Dcn protein, mouse ; DCN protein, human
    Language English
    Publishing date 2024-04-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2317760121
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Jg. 1995 - 2021: Lesesall (1.OG)
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  7. Article: Decorin suppresses tumor lymphangiogenesis: A mechanism to curtail cancer progression.

    Mondal, Dipon K / Xie, Christopher / Buraschi, Simone / Iozzo, Renato V

    bioRxiv : the preprint server for biology

    2023  

    Abstract: The complex interplay between malignant cells and the cellular and molecular components of the tumor stroma is a key aspect of cancer growth and development. These tumor-host interactions are often affected by soluble bioactive molecules such as ... ...

    Abstract The complex interplay between malignant cells and the cellular and molecular components of the tumor stroma is a key aspect of cancer growth and development. These tumor-host interactions are often affected by soluble bioactive molecules such as proteoglycans. Decorin, an archetypical small leucine-rich proteoglycan primarily expressed by stromal cells, affects cancer growth in its soluble form by interacting with several receptor tyrosine kinases (RTK). Overall, decorin leads to a context-dependent and protracted cessation of oncogenic RTK activity by attenuating their ability to drive a pro-survival program and to sustain a pro-angiogenic network. Through an unbiased transcriptomic analysis using deep RNAseq, we discovered that decorin downregulated a cluster of tumor-associated genes involved in lymphatic vessel development when systemically delivered to mice harboring breast carcinoma allografts. We found that Lyve1 and Podoplanin, two established markers of lymphatic vessels, were markedly suppressed at both the mRNA and protein levels and this suppression correlated with a significant reduction in tumor lymphatic vessels. We further discovered that soluble decorin, but not its homologous proteoglycan biglycan, inhibited lymphatic vessel sprouting in an
    Language English
    Publishing date 2023-08-29
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.08.28.555187
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  8. Article ; Online: Decorin evokes reversible mitochondrial depolarization in carcinoma and vascular endothelial cells.

    Neill, Thomas / Xie, Christopher / Iozzo, Renato V

    American journal of physiology. Cell physiology

    2022  Volume 323, Issue 5, Page(s) C1355–C1373

    Abstract: Decorin, a small leucine-rich proteoglycan with multiple biological functions, is known to evoke autophagy and mitophagy in both endothelial and cancer cells. Here, we investigated the effects of soluble decorin on mitochondrial homeostasis using live ... ...

    Abstract Decorin, a small leucine-rich proteoglycan with multiple biological functions, is known to evoke autophagy and mitophagy in both endothelial and cancer cells. Here, we investigated the effects of soluble decorin on mitochondrial homeostasis using live cell imaging and ex vivo angiogenic assays. We discovered that decorin triggers mitochondrial depolarization in triple-negative breast carcinoma, HeLa, and endothelial cells. This bioactivity was mediated by the protein core in a time- and dose-dependent manner and was specific for decorin insofar as biglycan, the closest homolog, failed to trigger depolarization. Mechanistically, we found that the bioactivity of decorin to promote depolarization required the MET receptor and its tyrosine kinase. Moreover, two mitochondrial interacting proteins, mitostatin and mitofusin 2, were essential for downstream decorin effects. Finally, we found that decorin relied on the canonical mitochondrial permeability transition pore to trigger tumor cell mitochondrial depolarization. Collectively, our study implicates decorin as a soluble outside-in regulator of mitochondrial dynamics.
    MeSH term(s) Humans ; Biglycan/pharmacology ; Carcinoma/metabolism ; Decorin/pharmacology ; Endothelial Cells/metabolism ; Extracellular Matrix Proteins/metabolism ; Mitochondrial Permeability Transition Pore ; Protein-Tyrosine Kinases/metabolism ; Signal Transduction
    Chemical Substances Biglycan ; Decorin ; Extracellular Matrix Proteins ; Mitochondrial Permeability Transition Pore ; Protein-Tyrosine Kinases (EC 2.7.10.1)
    Language English
    Publishing date 2022-08-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00325.2022
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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.89: Show issues Location:
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  9. Article ; Online: Angiostatic cues from the matrix: Endothelial cell autophagy meets hyaluronan biology.

    Chen, Carolyn G / Iozzo, Renato V

    The Journal of biological chemistry

    2020  Volume 295, Issue 49, Page(s) 16797–16812

    Abstract: The extracellular matrix encompasses a reservoir of bioactive macromolecules that modulates a cornucopia of biological functions. A prominent body of work posits matrix constituents as master regulators of autophagy and angiogenesis and provides ... ...

    Abstract The extracellular matrix encompasses a reservoir of bioactive macromolecules that modulates a cornucopia of biological functions. A prominent body of work posits matrix constituents as master regulators of autophagy and angiogenesis and provides molecular insight into how these two processes are coordinated. Here, we review current understanding of the molecular mechanisms underlying hyaluronan and HAS2 regulation and the role of soluble proteoglycan in affecting autophagy and angiogenesis. Specifically, we assess the role of proteoglycan-evoked autophagy in regulating angiogenesis via the HAS2-hyaluronan axis and ATG9A, a novel HAS2 binding partner. We discuss extracellular hyaluronan biology and the post-transcriptional and post-translational modifications that regulate its main synthesizer, HAS2. We highlight the emerging group of proteoglycans that utilize outside-in signaling to modulate autophagy and angiogenesis in cancer microenvironments and thoroughly review the most up-to-date understanding of endorepellin signaling in vascular endothelia, providing insight into the temporal complexities involved.
    MeSH term(s) Autophagy ; Autophagy-Related Proteins/metabolism ; Endothelium, Vascular/cytology ; Endothelium, Vascular/metabolism ; Humans ; Hyaluronan Synthases/metabolism ; Hyaluronic Acid/metabolism ; Neovascularization, Pathologic ; Signal Transduction ; Vascular Endothelial Growth Factor A/metabolism ; Vascular Endothelial Growth Factor Receptor-2/metabolism
    Chemical Substances Autophagy-Related Proteins ; Vascular Endothelial Growth Factor A ; Hyaluronic Acid (9004-61-9) ; Hyaluronan Synthases (EC 2.4.1.212) ; Vascular Endothelial Growth Factor Receptor-2 (EC 2.7.10.1)
    Language English
    Publishing date 2020-10-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.REV120.014391
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    Uc I Zs.108: Show issues Location:
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  10. Article ; Online: Progranulin and EGFR modulate receptor-like tyrosine kinase sorting and stability in mesothelioma cells.

    Ventura, Elisa / Belfiore, Antonino / Iozzo, Renato V / Giordano, Antonio / Morrione, Andrea

    American journal of physiology. Cell physiology

    2023  Volume 325, Issue 2, Page(s) C391–C405

    Abstract: Progranulin is a growth factor with pro-tumorigenic activity. We recently demonstrated that in mesothelioma, progranulin regulates cell migration, invasion, adhesion, and in vivo tumor formation by modulating a complex signaling network involving ... ...

    Abstract Progranulin is a growth factor with pro-tumorigenic activity. We recently demonstrated that in mesothelioma, progranulin regulates cell migration, invasion, adhesion, and in vivo tumor formation by modulating a complex signaling network involving multiple receptor tyrosine kinase (RTK)s. Progranulin biological activity relies on epidermal growth factor receptor (EGFR) and receptor-like tyrosine kinase (RYK), a co-receptor of the Wnt signaling pathway, which are both required for progranulin-induced downstream signaling. However, the molecular mechanism regulating the functional interaction among progranulin, EGFR, and RYK are not known. In this study, we demonstrated that progranulin directly interacted with RYK by specific enzyme-linked immunosorbent assay (ELISA) (K
    MeSH term(s) Humans ; Progranulins ; Receptor Protein-Tyrosine Kinases/metabolism ; ErbB Receptors/metabolism ; Wnt Signaling Pathway/physiology ; Cell Movement ; Intercellular Signaling Peptides and Proteins ; Mesothelioma
    Chemical Substances Progranulins ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1) ; Intercellular Signaling Peptides and Proteins ; EGFR protein, human (EC 2.7.10.1)
    Language English
    Publishing date 2023-07-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00248.2023
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