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  1. Article ; Online: Semaphorin Signaling in Cancer-Associated Inflammation.

    Franzolin, Giulia / Tamagnone, Luca

    International journal of molecular sciences

    2019  Volume 20, Issue 2

    Abstract: The inflammatory and immune response elicited by the growth of cancer cells is a major element conditioning the tumor microenvironment, impinging on disease progression and patients' prognosis. Semaphorin receptors are widely expressed in inflammatory ... ...

    Abstract The inflammatory and immune response elicited by the growth of cancer cells is a major element conditioning the tumor microenvironment, impinging on disease progression and patients' prognosis. Semaphorin receptors are widely expressed in inflammatory cells, and their ligands are provided by tumor cells, featuring an intense signaling cross-talk at local and systemic levels. Moreover, diverse semaphorins control both cells of the innate and the antigen-specific immunity. Notably, semaphorin signals acting as inhibitors of anti-cancer immune response are often dysregulated in human tumors, and may represent potential therapeutic targets. In this mini-review, we provide a survey of the best known semaphorin regulators of inflammatory and immune cells, and discuss their functional impact in the tumor microenvironment.
    MeSH term(s) Adaptive Immunity ; Animals ; Gene Expression Regulation ; Humans ; Immunity, Innate ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation/pathology ; Multigene Family ; Neoplasms/genetics ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/pathology ; Semaphorins/genetics ; Semaphorins/metabolism ; Signal Transduction ; Tumor Microenvironment/genetics ; Tumor Microenvironment/immunology
    Chemical Substances Semaphorins
    Language English
    Publishing date 2019-01-17
    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/ijms20020377
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Targeting Semaphorin 4D in Cancer: A Look from Different Perspectives.

    Tamagnone, Luca / Franzolin, Giulia

    Cancer research

    2019  Volume 79, Issue 20, Page(s) 5146–5148

    Abstract: Semaphorin 4D (Sema4D) plays a role in various cell types including B lymphocytes, differentiating neurons, endothelial cells, and cancer cells. Preclinical ... ...

    Abstract Semaphorin 4D (Sema4D) plays a role in various cell types including B lymphocytes, differentiating neurons, endothelial cells, and cancer cells. Preclinical and
    MeSH term(s) Antigens, CD ; Endothelial Cells ; Semaphorins ; Signal Transduction
    Chemical Substances Antigens, CD ; CD100 antigen ; Semaphorins
    Language English
    Publishing date 2019-10-01
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-19-2387
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.135/5: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Sema4C/PlexinB2 signaling controls breast cancer cell growth, hormonal dependence and tumorigenic potential.

    Gurrapu, Sreeharsha / Pupo, Emanuela / Franzolin, Giulia / Lanzetti, Letizia / Tamagnone, Luca

    Cell death and differentiation

    2018  Volume 25, Issue 7, Page(s) 1259–1275

    Abstract: Semaphorin 4C (Sema4C) expression in human breast cancers correlates with poor disease outcome. Surprisingly, upon knock-down of Sema4C or its receptor PlexinB2 in diverse mammary carcinoma cells (but not their normal counterparts), we observed dramatic ... ...

    Abstract Semaphorin 4C (Sema4C) expression in human breast cancers correlates with poor disease outcome. Surprisingly, upon knock-down of Sema4C or its receptor PlexinB2 in diverse mammary carcinoma cells (but not their normal counterparts), we observed dramatic growth inhibition associated with impairment of G2/M phase transition, cytokinesis defects and the onset of cell senescence. Mechanistically, we demonstrated a Sema4C/PlexinB2/LARG-dependent signaling cascade that is required to maintain critical RhoA-GTP levels in cancer cells. Interestingly, we also found that Sema4C upregulation in luminal-type breast cancer cells drives a dramatic phenotypic change, with disassembly of polarity complexes, mitotic spindle misorientation, cell-cell dissociation and increased migration and invasiveness. We found that this signaling cascade is dependent on the PlexinB2 effectors ErbB2 and RhoA-dependent kinases. Moreover, Sema4C-overexpressing luminal breast cancer cells upregulated the transcription factors Snail, Slug and SOX-2, and formed estrogen-independent metastatic tumors in mice. In sum, our data indicate that Sema4C/PlexinB2 signaling is essential for the growth of breast carcinoma cells, featuring a novel potential therapeutic target. In addition, elevated Sema4C expression enables indolent luminal-type tumors to become resistant to estrogen deprivation, invasive and metastatic in vivo, which could account for its association with a subset of human breast cancers with poor prognosis.
    MeSH term(s) Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Estrogens/metabolism ; Estrogens/pharmacology ; Female ; Humans ; MCF-7 Cells ; Mice ; Mice, Nude ; Mice, SCID ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Receptor, ErbB-2/genetics ; Receptor, ErbB-2/metabolism ; Semaphorins/genetics ; Semaphorins/metabolism ; Signal Transduction/drug effects ; Signal Transduction/genetics
    Chemical Substances Estrogens ; Nerve Tissue Proteins ; PLXNB2 protein, human ; Sema4c protein, human ; Semaphorins ; ERBB2 protein, human (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1)
    Language English
    Publishing date 2018-03-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1225672-9
    ISSN 1476-5403 ; 1350-9047
    ISSN (online) 1476-5403
    ISSN 1350-9047
    DOI 10.1038/s41418-018-0097-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4230: 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)
    Zs.MG 80: Show issues

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  4. Article ; Online: Mutated axon guidance gene PLXNB2 sustains growth and invasiveness of stem cells isolated from cancers of unknown primary.

    Brundu, Serena / Napolitano, Virginia / Franzolin, Giulia / Lo Cascio, Ettore / Mastrantonio, Roberta / Sardo, Gabriele / Cascardi, Eliano / Verginelli, Federica / Sarnataro, Sergio / Gambardella, Gennaro / Pisacane, Alberto / Arcovito, Alessandro / Boccaccio, Carla / Comoglio, Paolo M / Giraudo, Enrico / Tamagnone, Luca

    EMBO molecular medicine

    2023  Volume 15, Issue 3, Page(s) e16104

    Abstract: The genetic changes sustaining the development of cancers of unknown primary (CUP) remain elusive. The whole-exome genomic profiling of 14 rigorously selected CUP samples did not reveal specific recurring mutation in known driver genes. However, by ... ...

    Abstract The genetic changes sustaining the development of cancers of unknown primary (CUP) remain elusive. The whole-exome genomic profiling of 14 rigorously selected CUP samples did not reveal specific recurring mutation in known driver genes. However, by comparing the mutational landscape of CUPs with that of most other human tumor types, it emerged a consistent enrichment of changes in genes belonging to the axon guidance KEGG pathway. In particular, G842C mutation of PlexinB2 (PlxnB2) was predicted to be activating. Indeed, knocking down the mutated, but not the wild-type, PlxnB2 in CUP stem cells resulted in the impairment of self-renewal and proliferation in culture, as well as tumorigenic capacity in mice. Conversely, the genetic transfer of G842C-PlxnB2 was sufficient to promote CUP stem cell proliferation and tumorigenesis in mice. Notably, G842C-PlxnB2 expression in CUP cells was associated with basal EGFR phosphorylation, and EGFR blockade impaired the viability of CUP cells reliant on the mutated receptor. Moreover, the mutated PlxnB2 elicited CUP cell invasiveness, blocked by EGFR inhibitor treatment. In sum, we found that a novel activating mutation of the axon guidance gene PLXNB2 sustains proliferative autonomy and confers invasive properties to stem cells isolated from cancers of unknown primary, in EGFR-dependent manner.
    MeSH term(s) Animals ; Humans ; Mice ; Axon Guidance ; ErbB Receptors/genetics ; Mutation ; Neoplasm Recurrence, Local ; Neoplasms, Unknown Primary/genetics ; Nerve Tissue Proteins/genetics ; Neoplastic Stem Cells/pathology
    Chemical Substances ErbB Receptors (EC 2.7.10.1) ; PLXNB2 protein, human ; Plxnb2 protein, mouse ; Nerve Tissue Proteins
    Language English
    Publishing date 2023-02-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2467145-9
    ISSN 1757-4684 ; 1757-4676
    ISSN (online) 1757-4684
    ISSN 1757-4676
    DOI 10.15252/emmm.202216104
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6784: Show issues Location:
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  5. Article ; Online: Reverse signaling by semaphorin 4C elicits SMAD1/5- and ID1/3-dependent invasive reprogramming in cancer cells.

    Gurrapu, Sreeharsha / Franzolin, Giulia / Fard, Damon / Accardo, Massimo / Medico, Enzo / Sarotto, Ivana / Sapino, Anna / Isella, Claudio / Tamagnone, Luca

    Science signaling

    2019  Volume 12, Issue 595

    Abstract: Semaphorins are a family of molecular signals that guide cell migration and are implicated in the regulation of cancer cells. In particular, transmembrane semaphorins are postulated to act as both ligands ("forward" mode) and signaling receptors (" ... ...

    Abstract Semaphorins are a family of molecular signals that guide cell migration and are implicated in the regulation of cancer cells. In particular, transmembrane semaphorins are postulated to act as both ligands ("forward" mode) and signaling receptors ("reverse" mode); however, reverse semaphorin signaling in cancer is relatively less understood. Here, we identified a previously unknown function of transmembrane semaphorin 4C (Sema4C), acting in reverse mode, to elicit nonconventional TGF-β/BMP receptor activation and selective SMAD1/5 phosphorylation. Sema4C coimmunoprecipitated with TGFBRII and BMPR1, supporting its role as modifier of this pathway. Sema4C reverse signaling led to the increased abundance of ID1/3 transcriptional factors and to extensive reprogramming of gene expression, which suppressed the typical features of the epithelial-mesenchymal transition in invasive carcinoma cells. This phenotype was nevertheless coupled with burgeoning metastatic behavior in vivo, consistent with evidence that Sema4C expression correlates with metastatic progression in human breast cancers. Thus, Sema4C reverse signaling promoted SMAD1/5- and ID1/3-dependent gene expression reprogramming and phenotypic plasticity in invasive cancer cells.
    MeSH term(s) Animals ; COS Cells ; Chlorocebus aethiops ; Humans ; Inhibitor of Differentiation Protein 1/genetics ; Inhibitor of Differentiation Protein 1/metabolism ; Inhibitor of Differentiation Proteins/genetics ; Inhibitor of Differentiation Proteins/metabolism ; Neoplasm Invasiveness ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; PC-3 Cells ; Semaphorins/genetics ; Semaphorins/metabolism ; Signal Transduction ; Smad1 Protein/genetics ; Smad1 Protein/metabolism ; Smad3 Protein/genetics ; Smad3 Protein/metabolism
    Chemical Substances ID1 protein, human ; Inhibitor of Differentiation Protein 1 ; Inhibitor of Differentiation Proteins ; Neoplasm Proteins ; SMAD1 protein, human ; SMAD3 protein, human ; Sema4c protein, human ; Semaphorins ; Smad1 Protein ; Smad3 Protein ; ID3 protein, human (147785-34-0)
    Language English
    Publishing date 2019-08-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2417226-1
    ISSN 1937-9145 ; 1945-0877
    ISSN (online) 1937-9145
    ISSN 1945-0877
    DOI 10.1126/scisignal.aav2041
    Database MEDical Literature Analysis and Retrieval System OnLINE

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