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  1. Article ; Online: Modeling metastasis in mice: a closer look.

    Giacobbe, Arianna / Abate-Shen, Cory

    Trends in cancer

    2021  Volume 7, Issue 10, Page(s) 916–929

    Abstract: Unraveling the multifaceted cellular and physiological processes associated with metastasis is best achieved by using in vivo models that recapitulate the requisite tumor cell-intrinsic and -extrinsic mechanisms at the organismal level. We discuss the ... ...

    Abstract Unraveling the multifaceted cellular and physiological processes associated with metastasis is best achieved by using in vivo models that recapitulate the requisite tumor cell-intrinsic and -extrinsic mechanisms at the organismal level. We discuss the current status of mouse models of metastasis. We consider how mouse models can refine our understanding of the underlying biological and molecular processes that promote metastasis, and we envisage how the application of new technologies will further enhance investigations of metastasis at single-cell resolution in the context of the whole organism. Our view is that investigations based on state-of-the-art mouse models can propel a holistic understanding of the biology of metastasis, which will ultimately lead to the discovery of new therapeutic opportunities.
    MeSH term(s) Animals ; Disease Models, Animal ; Mice ; Neoplasms
    Language English
    Publishing date 2021-07-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2852626-0
    ISSN 2405-8025 ; 2405-8033 ; 2405-8033
    ISSN (online) 2405-8025 ; 2405-8033
    ISSN 2405-8033
    DOI 10.1016/j.trecan.2021.06.010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: NSD2 is a conserved driver of metastatic prostate cancer progression.

    Aytes, Alvaro / Giacobbe, Arianna / Mitrofanova, Antonina / Ruggero, Katia / Cyrta, Joanna / Arriaga, Juan / Palomero, Luis / Farran-Matas, Sonia / Rubin, Mark A / Shen, Michael M / Califano, Andrea / Abate-Shen, Cory

    Nature communications

    2018  Volume 9, Issue 1, Page(s) 5201

    Abstract: Deciphering cell-intrinsic mechanisms of metastasis progression in vivo is essential to identify novel therapeutic approaches. Here we elucidate cell-intrinsic drivers of metastatic prostate cancer progression through analyses of genetically engineered ... ...

    Abstract Deciphering cell-intrinsic mechanisms of metastasis progression in vivo is essential to identify novel therapeutic approaches. Here we elucidate cell-intrinsic drivers of metastatic prostate cancer progression through analyses of genetically engineered mouse models (GEMM) and correlative studies of human prostate cancer. Expression profiling of lineage-marked cells from mouse primary tumors and metastases defines a signature of de novo metastatic progression. Cross-species master regulator analyses comparing this mouse signature with a comparable human signature identifies conserved drivers of metastatic progression with demonstrable clinical and functional relevance. In particular, nuclear receptor binding SET Domain Protein 2 (NSD2) is robustly expressed in lethal prostate cancer in humans, while its silencing inhibits metastasis of mouse allografts in vivo. We propose that cross-species analysis can elucidate mechanisms of metastasis progression, thus providing potential additional therapeutic opportunities for treatment of lethal prostate cancer.
    MeSH term(s) Animals ; Cell Line, Tumor ; Disease Progression ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Histone-Lysine N-Methyltransferase/genetics ; Histone-Lysine N-Methyltransferase/metabolism ; Humans ; Male ; Mice ; Mice, Nude ; Neoplasm Metastasis ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Repressor Proteins/genetics ; Repressor Proteins/metabolism
    Chemical Substances RNA, Small Interfering ; Repressor Proteins ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; NSD2 protein, human (EC 2.1.1.43) ; WHSC1 protein, mouse (EC 2.1.1.43)
    Language English
    Publishing date 2018-12-05
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-018-07511-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Anti-tumoral effect of desmethylclomipramine in lung cancer stem cells.

    Bongiorno-Borbone, Lucilla / Giacobbe, Arianna / Compagnone, Mirco / Eramo, Adriana / De Maria, Ruggero / Peschiaroli, Angelo / Melino, Gerry

    Oncotarget

    2015  Volume 6, Issue 19, Page(s) 16926–16938

    Abstract: Lung cancer is the most feared of all cancers because of its heterogeneity and resistance to available treatments. Cancer stem cells (CSCs) are the cell population responsible for lung cancer chemoresistance and are a very good model for testing new ... ...

    Abstract Lung cancer is the most feared of all cancers because of its heterogeneity and resistance to available treatments. Cancer stem cells (CSCs) are the cell population responsible for lung cancer chemoresistance and are a very good model for testing new targeted therapies. Clomipramine is an FDA-approved antidepressant drug, able to inhibit in vitro the E3 ubiquitin ligase Itch and potentiate the pro-apoptotic effects of DNA damaging induced agents in several cancer cell lines. Here, we investigated the potential therapeutic effect of desmethylclomipramine (DCMI), the active metabolite of Clomipramine, on the CSCs homeostasis. We show that DCMI inhibits lung CSCs growth, decreases their stemness potential and increases the cytotoxic effect of conventional chemotherapeutic drugs. Being DCMI an inhibitor of the E3 ubiquitin ligase Itch, we also verified the effect of Itch deregulation on CSCs survival. We found that the siRNA-mediated depletion of Itch induces similar anti-proliferative effects on lung CSCs, suggesting that DCMI might exert its effect, at least in part, by inhibiting Itch. Notably, Itch expression is a negative prognostic factor in two primary lung tumors datasets, supporting the potential clinical relevance of Itch inhibition to circumvent drug resistance in the treatment of lung cancer.
    MeSH term(s) Adenocarcinoma/genetics ; Adenocarcinoma/mortality ; Adenocarcinoma/pathology ; Antineoplastic Agents/pharmacology ; Blotting, Western ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cells, Cultured ; Clomipramine/analogs & derivatives ; Clomipramine/pharmacology ; Drug Resistance, Neoplasm/drug effects ; Flow Cytometry ; Humans ; Kaplan-Meier Estimate ; Lung Neoplasms/genetics ; Lung Neoplasms/mortality ; Lung Neoplasms/pathology ; Neoplastic Stem Cells/drug effects ; RNA Interference ; Repressor Proteins/genetics ; Ubiquitin-Protein Ligases/genetics
    Chemical Substances Antineoplastic Agents ; Repressor Proteins ; desmethylclomipramine (01DN47PPQG) ; ITCH protein, human (EC 2.3.2.26) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Clomipramine (NUV44L116D)
    Language English
    Publishing date 2015-07-25
    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.4700
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: p63 Sustains self-renewal of mammary cancer stem cells through regulation of Sonic Hedgehog signaling.

    Memmi, Elisa Maria / Sanarico, Anna Giulia / Giacobbe, Arianna / Peschiaroli, Angelo / Frezza, Valentina / Cicalese, Angelo / Pisati, Federica / Tosoni, Daniela / Zhou, Huiqing / Tonon, Giovanni / Antonov, Alexey / Melino, Gerry / Pelicci, Pier Giuseppe / Bernassola, Francesca

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

    2015  Volume 112, Issue 11, Page(s) 3499–3504

    Abstract: The predominant p63 isoform, ΔNp63, is a master regulator of normal epithelial stem cell (SC) maintenance. However, in vivo evidence of the regulation of cancer stem cell (CSC) properties by p63 is still limited. Here, we exploit the transgenic MMTV- ... ...

    Abstract The predominant p63 isoform, ΔNp63, is a master regulator of normal epithelial stem cell (SC) maintenance. However, in vivo evidence of the regulation of cancer stem cell (CSC) properties by p63 is still limited. Here, we exploit the transgenic MMTV-ErbB2 (v-erb-b2 avian erythroblastic leukemia viral oncogene homolog 2) mouse model of carcinogenesis to dissect the role of p63 in the regulation of mammary CSC self-renewal and breast tumorigenesis. ErbB2 tumor cells enriched for SC-like properties display increased levels of ΔNp63 expression compared with normal mammary progenitors. Down-regulation of p63 in ErbB2 mammospheres markedly restricts self-renewal and expansion of CSCs, and this action is fully independent of p53. Furthermore, transplantation of ErbB2 progenitors expressing shRNAs against p63 into the mammary fat pads of syngeneic mice delays tumor growth in vivo. p63 knockdown in ErbB2 progenitors diminishes the expression of genes encoding components of the Sonic Hedgehog (Hh) signaling pathway, a driver of mammary SC self-renewal. Remarkably, p63 regulates the expression of Sonic Hedgehog (Shh), GLI family zinc finger 2 (Gli2), and Patched1 (Ptch1) genes by directly binding to their gene regulatory regions, and eventually contributes to pathway activation. Collectively, these studies highlight the importance of p63 in maintaining the self-renewal potential of mammary CSCs via a positive modulation of the Hh signaling pathway.
    MeSH term(s) Animals ; Cell Proliferation ; Female ; Gene Expression Regulation, Neoplastic ; Hedgehog Proteins/metabolism ; Mammary Glands, Animal/pathology ; Mammary Neoplasms, Experimental/genetics ; Mammary Neoplasms, Experimental/pathology ; Mice, Inbred C57BL ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Receptor, ErbB-2/metabolism ; Signal Transduction/genetics ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Transcription, Genetic
    Chemical Substances Hedgehog Proteins ; Phosphoproteins ; Shh protein, mouse ; Trans-Activators ; Trp63 protein, mouse ; Erbb2 protein, mouse (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1)
    Language English
    Publishing date 2015-03-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1500762112
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1148: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
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  5. Article ; Online: A MYC and RAS co-activation signature in localized prostate cancer drives bone metastasis and castration resistance.

    Arriaga, Juan M / Panja, Sukanya / Alshalalfa, Mohammed / Zhao, Junfei / Zou, Min / Giacobbe, Arianna / Madubata, Chioma J / Kim, Jaime Yeji / Rodriguez, Antonio / Coleman, Ilsa / Virk, Renu K / Hibshoosh, Hanina / Ertunc, Onur / Ozbek, Büşra / Fountain, Julia / Jeffrey Karnes, R / Luo, Jun / Antonarakis, Emmanuel S / Nelson, Peter S /
    Feng, Felix Y / Rubin, Mark A / De Marzo, Angelo M / Rabadan, Raul / Sims, Peter A / Mitrofanova, Antonina / Abate-Shen, Cory

    Nature cancer

    2020  Volume 1, Issue 11, Page(s) 1082–1096

    Abstract: Understanding the intricacies of lethal prostate cancer poses specific challenges due to difficulties in accurate modeling of metastasis in vivo. Here we show ... ...

    Abstract Understanding the intricacies of lethal prostate cancer poses specific challenges due to difficulties in accurate modeling of metastasis in vivo. Here we show that
    MeSH term(s) Animals ; Bone Neoplasms/genetics ; Castration ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Mice ; Prostatic Neoplasms/genetics ; Transcription Factors/genetics
    Chemical Substances Transcription Factors
    Language English
    Publishing date 2020-10-19
    Publishing country England
    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.
    ISSN 2662-1347
    ISSN (online) 2662-1347
    DOI 10.1038/s43018-020-00125-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: p63 regulates glutaminase 2 expression.

    Giacobbe, Arianna / Bongiorno-Borbone, Lucilla / Bernassola, Francesca / Terrinoni, Alessandro / Markert, Elke Katrin / Levine, Arnold J / Feng, Zhaohui / Agostini, Massimilano / Zolla, Lello / Agrò, Alessandro Finazzi / Notterman, Daniel A / Melino, Gerry / Peschiaroli, Angelo

    Cell cycle (Georgetown, Tex.)

    2013  Volume 12, Issue 9, Page(s) 1395–1405

    Abstract: The transcription factor p63 is critical for many biological processes, including development and maintenance of epidermal tissues and tumorigenesis. Here, we report that the TAp63 isoforms regulate cell metabolism through the induction of the ... ...

    Abstract The transcription factor p63 is critical for many biological processes, including development and maintenance of epidermal tissues and tumorigenesis. Here, we report that the TAp63 isoforms regulate cell metabolism through the induction of the mitochondrial glutaminase 2 (GLS2) gene both in primary cells and tumor cell lines. By ChIP analysis and luciferase assay, we confirmed that TAp63 binds directly to the p53/p63 consensus DNA binding sequence within the GLS2 promoter region. Given the critical role of p63 in epidermal differentiation, we have investigated the regulation of GLS2 expression during this process. GLS2 and TAp63 expression increases during the in vitro differentiation of primary human keratinocytes, and depletion of GLS2 inhibits skin differentiation both at molecular and cellular levels. We found that GLS2 and TAp63 expression are concomitantly induced in cancer cells exposed to oxidative stresses. siRNA-mediated depletion of GLS2 sensitizes cells to ROS-induced apoptosis, suggesting that the TAp63/GLS2 axis can be functionally important as a cellular antioxidant pathway in the absence of p53. Accordingly, we found that GLS2 is upregulated in colon adenocarcinoma. Altogether, our findings demonstrate that GLS2 is a bona fide TAp63 target gene, and that the TAp63-dependent regulation of GLS2 is important for both physiological and pathological processes.
    MeSH term(s) Adenocarcinoma/enzymology ; Adenocarcinoma/pathology ; Apoptosis/drug effects ; Cell Differentiation/drug effects ; Cell Line, Tumor ; Colonic Neoplasms/enzymology ; Colonic Neoplasms/pathology ; Cytoprotection/drug effects ; DNA Damage ; Glutaminase/genetics ; Glutaminase/metabolism ; Histone Deacetylase Inhibitors/pharmacology ; Humans ; Keratinocytes/cytology ; Keratinocytes/metabolism ; Reactive Oxygen Species/metabolism ; Skin/cytology ; Stress, Physiological/drug effects ; Transcription Factors/metabolism ; Tumor Suppressor Proteins/metabolism ; Up-Regulation/drug effects
    Chemical Substances Histone Deacetylase Inhibitors ; Reactive Oxygen Species ; TP63 protein, human ; Transcription Factors ; Tumor Suppressor Proteins ; Glutaminase (EC 3.5.1.2)
    Language English
    Publishing date 2013-04-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.4161/cc.24478
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5881: 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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