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  1. Article ; Online: Protocol to screen for Sorafenib resistance regulators using pooled lentiviral shRNA library and a Sorafenib-resistant hepatocellular carcinoma cell model.

    Gao, Ruize / Tang, Fengyuan / Christofori, Gerhard

    STAR protocols

    2023  Volume 4, Issue 2, Page(s) 102273

    Abstract: Approaches to study therapy resistance in HCC (hepatocellular carcinoma) are limited, especially when using HCC models in vitro. Here, we present a protocol to establish an in vitro Sorafenib-resistant human HCC cell model and conduct an shRNA-mediated ... ...

    Abstract Approaches to study therapy resistance in HCC (hepatocellular carcinoma) are limited, especially when using HCC models in vitro. Here, we present a protocol to establish an in vitro Sorafenib-resistant human HCC cell model and conduct an shRNA-mediated synthetic lethal screen in established Sorafenib-resistant HCC cell lines to identify critical regulators of Sorafenib resistance. We describe steps for RNA sequencing and functional analysis to reveal the mode of action of potential candidates in conferring therapy resistance to HCC cells. For complete details on the use and execution of this protocol, please refer to Gao et al. (2021a)
    Language English
    Publishing date 2023-04-30
    Publishing country United States
    Document type Journal Article
    ISSN 2666-1667
    ISSN (online) 2666-1667
    DOI 10.1016/j.xpro.2023.102273
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: LATS1-Beclin1 mediates a non-canonical connection between the Hippo pathway and autophagy.

    Tang, Fengyuan / Christofori, Gerhard

    Molecular & cellular oncology

    2020  Volume 7, Issue 4, Page(s) 1757378

    Abstract: Understanding the mechanisms of evasive resistance in cancer is of great importance to develop efficient therapies. Analyzing the molecular mechanisms underlying therapy resistance of hepatocellular carcinoma (HCC), we have discovered a kinase-activity ... ...

    Abstract Understanding the mechanisms of evasive resistance in cancer is of great importance to develop efficient therapies. Analyzing the molecular mechanisms underlying therapy resistance of hepatocellular carcinoma (HCC), we have discovered a kinase-activity independent role of LATS1 (large tumor suppressor) but not LATS2 in regulating sorafenib-induced lethal autophagy in HCC. We have found that the autophagy regulatory role of LATS1 is a general phenomenon in response to various stimuli of autophagy induction which relies on a LATS1-specific protein domain. Mechanistically, the autophagy regulatory role of LATS1 is coupled with Beclin-1 (BECN1) K27-linked ubiquitination and BECN1 self-dimerization. Our study highlights a LATS1-mediated non-classical interaction between the Hippo signaling pathway and autophagy in therapy response and carcinogenesis.
    Language English
    Publishing date 2020-05-13
    Publishing country United States
    Document type Journal Article
    ISSN 2372-3556
    ISSN 2372-3556
    DOI 10.1080/23723556.2020.1757378
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  3. Article ; Online: The cross-talk between the Hippo signaling pathway and autophagy:implications on physiology and cancer.

    Tang, Fengyuan / Christofori, Gerhard

    Cell cycle (Georgetown, Tex.)

    2020  Volume 19, Issue 20, Page(s) 2563–2572

    Abstract: Organ development is precisely guided by spatiotemporal cross-talks between a variety of signaling pathways regulating cell differentiation, proliferation, growth arrest and physiological cell death. Aberrant signaling inputs invariably lead to tissue ... ...

    Abstract Organ development is precisely guided by spatiotemporal cross-talks between a variety of signaling pathways regulating cell differentiation, proliferation, growth arrest and physiological cell death. Aberrant signaling inputs invariably lead to tissue dysfunction and to certain conditions, even malignant transformation. In this review, we focus on the functional interplay between the Hippo signaling pathway and autophagy in normal tissue homeostasis and in malignant tumor progression. Mounting experimental evidence for the regulation of cancer cell malignancy and therapy resistance by the functional cross-talk between Hippo signaling and autophagy highlights this signaling axis as a suitable therapeutic target to combat cancer.
    MeSH term(s) Animals ; Autophagy/physiology ; Cell Differentiation/physiology ; Cell Proliferation/physiology ; Hippo Signaling Pathway/physiology ; Homeostasis/physiology ; Humans ; Neoplasms/metabolism ; Neoplasms/pathology
    Language English
    Publishing date 2020-08-18
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.1080/15384101.2020.1806450
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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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  4. Article ; Online: Breast cancer as an example of tumour heterogeneity and tumour cell plasticity during malignant progression.

    Lüönd, Fabiana / Tiede, Stefanie / Christofori, Gerhard

    British journal of cancer

    2021  Volume 125, Issue 2, Page(s) 164–175

    Abstract: Heterogeneity within a tumour increases its ability to adapt to constantly changing constraints, but adversely affects a patient's prognosis, therapy response and clinical outcome. Intratumoural heterogeneity results from a combination of extrinsic ... ...

    Abstract Heterogeneity within a tumour increases its ability to adapt to constantly changing constraints, but adversely affects a patient's prognosis, therapy response and clinical outcome. Intratumoural heterogeneity results from a combination of extrinsic factors from the tumour microenvironment and intrinsic parameters from the cancer cells themselves, including their genetic, epigenetic and transcriptomic traits, their ability to proliferate, migrate and invade, and their stemness and plasticity attributes. Cell plasticity constitutes the ability of cancer cells to rapidly reprogramme their gene expression repertoire, to change their behaviour and identities, and to adapt to microenvironmental cues. These features also directly contribute to tumour heterogeneity and are critical for malignant tumour progression. In this article, we use breast cancer as an example of the origins of tumour heterogeneity (in particular, the mutational spectrum and clonal evolution of progressing tumours) and of tumour cell plasticity (in particular, that shown by tumour cells undergoing epithelial-to-mesenchymal transition), as well as considering interclonal cooperativity and cell plasticity as sources of cancer cell heterogeneity. We review current knowledge on the functional contribution of cell plasticity and tumour heterogeneity to malignant tumour progression, metastasis formation and therapy resistance.
    MeSH term(s) Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Plasticity ; Disease Progression ; Drug Resistance, Neoplasm ; Epigenesis, Genetic ; Epithelial-Mesenchymal Transition ; Female ; Gene Expression Regulation, Neoplastic ; Gene Regulatory Networks ; Genetic Heterogeneity ; Humans
    Language English
    Publishing date 2021-04-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80075-2
    ISSN 1532-1827 ; 0007-0920
    ISSN (online) 1532-1827
    ISSN 0007-0920
    DOI 10.1038/s41416-021-01328-7
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    Uh III Zs.142: 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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  5. Article ; Online: Targeting Cancer Cell Metastasis by Converting Cancer Cells into Fat.

    Ishay-Ronen, Dana / Christofori, Gerhard

    Cancer research

    2019  Volume 79, Issue 21, Page(s) 5471–5475

    Abstract: Cancer is a systemic heterogeneous disease that can undergo several rounds of latency and activation. Malignant tumors evolve through dynamic responses to microenvironmental signals and development of resistance following therapeutic interventions. ... ...

    Abstract Cancer is a systemic heterogeneous disease that can undergo several rounds of latency and activation. Malignant tumors evolve through dynamic responses to microenvironmental signals and development of resistance following therapeutic interventions. Cancer cell adaptation is required for cell survival during metastatic dissemination and outgrowth. Epithelial-mesenchymal transition (EMT) plays a major role in facilitating cell plasticity in cancer and allows cancer cells to escape chemotherapies and targeted therapies through dedifferentiation and signaling adaptation processes. In our recent study, we showed that breast cancer cells that have undergone EMT can be terminally differentiated into adipocytes using the PPARγ agonist rosiglitazone combined with the MEK inhibitor trametinib. The conversion of invasive cancer cells into adipocytes repressed primary tumor invasion and metastasis formation in mouse models of breast cancer. The transdifferentiated cancer cell-derived adipocytes were growth-arrested and lost their cellular plasticity. These results indicate the high potential of utilizing the increased cell plasticity inherent to invasive cancer cells for transdifferentiation therapy.
    MeSH term(s) Adipocytes/pathology ; Animals ; Breast Neoplasms/pathology ; Cell Differentiation/physiology ; Cell Transdifferentiation/physiology ; Epithelial-Mesenchymal Transition/physiology ; Female ; Humans ; Neoplasm Metastasis/pathology
    Language English
    Publishing date 2019-07-22
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-19-1242
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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.135/5: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  6. Article ; Online: Metastatic colon cancer cells negotiate the intravasation Notch.

    Christofori, Gerhard

    Cancer cell

    2011  Volume 19, Issue 1, Page(s) 6–8

    Abstract: In this issue of Cancer Cell, Sonoshita et al. report that Aes/Grg5 prevents metastasis of colorectal cancer cells by sequestering and inactivating Notch transcriptional effectors in distinct nuclear foci. Loss of Aes/Grg5 in invasive cancer cells where ... ...

    Abstract In this issue of Cancer Cell, Sonoshita et al. report that Aes/Grg5 prevents metastasis of colorectal cancer cells by sequestering and inactivating Notch transcriptional effectors in distinct nuclear foci. Loss of Aes/Grg5 in invasive cancer cells where Notch is activated by stroma-expressed ligands promotes invasion, transendothelial migration, intravasation, and metastasis.
    Language English
    Publishing date 2011-01-18
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 2078448-X
    ISSN 1878-3686 ; 1535-6108
    ISSN (online) 1878-3686
    ISSN 1535-6108
    DOI 10.1016/j.ccr.2011.01.003
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5650: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
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    Zs.MG 104: Show issues

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  7. Article ; Online: Snail1 links transcriptional control with epigenetic regulation.

    Christofori, Gerhard

    The EMBO journal

    2010  Volume 29, Issue 11, Page(s) 1787–1789

    MeSH term(s) Animals ; Gene Expression Regulation ; Humans ; Promoter Regions, Genetic
    Language English
    Publishing date 2010-06-02
    Publishing country England
    Document type Comment ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 586044-1
    ISSN 1460-2075 ; 0261-4189
    ISSN (online) 1460-2075
    ISSN 0261-4189
    DOI 10.1038/emboj.2010.92
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    Zs.A 1808: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 100: Show issues

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  8. Article ; Online: Reciprocal regulatory circuits coordinating EMT plasticity.

    Diepenbruck, Maren / Christofori, Gerhard

    Cell stress

    2017  Volume 1, Issue 3, Page(s) 139–140

    Abstract: Epithelial to mesenchymal transition (EMT) as well as its reversal process, mesenchymal to epithelial transition (MET), are essential and well-controlled cellular processes during embryonic development. Tightly controlled regulatory mechanisms guide an ... ...

    Abstract Epithelial to mesenchymal transition (EMT) as well as its reversal process, mesenchymal to epithelial transition (MET), are essential and well-controlled cellular processes during embryonic development. Tightly controlled regulatory mechanisms guide an EMT/MET plasticity and enable cells to switch forth and back between different cell morphologies and functional capabilities to endow the necessity of tissue plasticity. However, aberrant and uncontrolled activation of these processes during malignant tumor progression promotes primary tumor cell invasion, cancer cell dissemination and metastatic outgrowth. In a recent study (Nat Commun; doi: 10.1038/s41467-017-01197-w), we have reported on the post-transcriptional control of normal and cancer-associated EMT by miRNAs and identified a novel, critical double-negative feedback regulation of the thus far unknown miRNA miR1199 and the key EMT transcription factor Zeb1.
    Language English
    Publishing date 2017-12-01
    Publishing country Austria
    Document type Journal Article ; Comment
    ISSN 2523-0204
    ISSN (online) 2523-0204
    DOI 10.15698/cst2017.12.117
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  9. Article ; Online: Author Correction: PyMT-1099, a versatile murine cell model for EMT in breast cancer.

    Saxena, Meera / Kalathur, Ravi Kiran Reddy / Neutzner, Melanie / Christofori, Gerhard

    Scientific reports

    2020  Volume 10, Issue 1, Page(s) 11444

    Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper. ...

    Abstract An amendment to this paper has been published and can be accessed via a link at the top of the paper.
    Language English
    Publishing date 2020-07-07
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-020-68523-z
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  10. Article ; Online: The Rip1Tag2 Transgenic Mouse Model.

    Bill, Ruben / Christofori, Gerhard

    Methods in molecular biology (Clifton, N.J.)

    2016  Volume 1464, Page(s) 151–161

    Abstract: The Rip1Tag2 transgenic mouse model of β-cell carcinogenesis has been instrumental in studying various aspects of tumor angiogenesis and in investigating the response to anti-angiogenic therapeutics. Thereby, the in-depth assessment of blood and ... ...

    Abstract The Rip1Tag2 transgenic mouse model of β-cell carcinogenesis has been instrumental in studying various aspects of tumor angiogenesis and in investigating the response to anti-angiogenic therapeutics. Thereby, the in-depth assessment of blood and lymphatic vessel phenotypes and functionality represents key experimental analyses. In this chapter, we describe basic protocols to assess tumor blood vessel morphology (pericyte coverage), functionality (perfusion, leakiness, and hypoxia), lymphatic tumor coverage, and tumor cell proliferation and apoptosis based on immunofluorescence microscopy analysis.
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-4939-3999-2_14
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