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  1. Article ; Online: The Oncogenic Protein Kinase/ATPase RIOK1 Is Up-Regulated via the c-myc/E2F Transcription Factor Axis in Prostate Cancer.

    Handle, Florian / Puhr, Martin / Gruber, Martina / Andolfi, Chiara / Schäfer, Georg / Klocker, Helmut / Haybaeck, Johannes / De Wulf, Peter / Culig, Zoran

    The American journal of pathology

    2023  Volume 193, Issue 9, Page(s) 1284–1297

    Abstract: The atypical protein kinase/ATPase RIO kinase (RIOK)-1 is involved in pre-40S ribosomal subunit production, cell-cycle progression, and protein arginine N-methyltransferase 5 methylosome substrate recruitment. RIOK1 overexpression is a characteristic of ... ...

    Abstract The atypical protein kinase/ATPase RIO kinase (RIOK)-1 is involved in pre-40S ribosomal subunit production, cell-cycle progression, and protein arginine N-methyltransferase 5 methylosome substrate recruitment. RIOK1 overexpression is a characteristic of several malignancies and is correlated with cancer stage, therapy resistance, poor patient survival, and other prognostic factors. However, its role in prostate cancer (PCa) is unknown. In this study, the expression, regulation, and therapeutic potential of RIOK1 in PCa were examined. RIOK1 mRNA and protein expression were elevated in PCa tissue samples and correlated with proliferative and protein homeostasis-related pathways. RIOK1 was identified as a downstream target gene of the c-myc/E2F transcription factors. Proliferation of PCa cells was significantly reduced with RIOK1 knockdown and overexpression of the dominant-negative RIOK1-D324A mutant. Biochemical inhibition of RIOK1 with toyocamycin led to strong antiproliferative effects in androgen receptor-negative and -positive PCa cell lines with EC
    MeSH term(s) Male ; Humans ; Genes, myc ; Protein Kinases/genetics ; Adenosine Triphosphatases/genetics ; Adenosine Triphosphatases/metabolism ; Adenosine Triphosphatases/pharmacology ; Toyocamycin/pharmacology ; Toyocamycin/therapeutic use ; Cell Proliferation ; Prostatic Neoplasms/pathology ; E2F Transcription Factors/genetics ; E2F Transcription Factors/metabolism ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic
    Chemical Substances Protein Kinases (EC 2.7.-) ; Adenosine Triphosphatases (EC 3.6.1.-) ; Toyocamycin (L7995C4D7F) ; E2F Transcription Factors
    Language English
    Publishing date 2023-06-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2943-9
    ISSN 1525-2191 ; 0002-9440
    ISSN (online) 1525-2191
    ISSN 0002-9440
    DOI 10.1016/j.ajpath.2023.05.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The stem cell inhibitor salinomycin decreases colony formation potential and tumor-initiating population in docetaxel-sensitive and docetaxel-resistant prostate cancer cells.

    Gruber, Martina / Handle, Florian / Culig, Zoran

    The Prostate

    2019  Volume 80, Issue 3, Page(s) 267–273

    Abstract: Background: Prostate cancer (PCa) is one of the most frequently diagnosed tumors in men. In general, therapies for localized PCa are curative. However, treatment of advanced PCa is considered palliative since development of therapy resistance occurs ... ...

    Abstract Background: Prostate cancer (PCa) is one of the most frequently diagnosed tumors in men. In general, therapies for localized PCa are curative. However, treatment of advanced PCa is considered palliative since development of therapy resistance occurs rapidly. It has been shown that tumor-initiating cells are likely involved in therapy resistance. They are not eliminated by conventional therapies and thereby lead to tumor progression and relapse. The aim of this study was to evaluate the effects of the known stem cell inhibitor salinomycin on this critical subpopulation of cells.
    Methods: Expression of the cell surface markers CD24 and CD44 was assessed by immunofluorescence and fluorescence-activated cell sorting. Colony formation efficiency and classification of colony types with varying tumor-initiating potential (holoclones, meroclones, and paraclones) were analyzed in an automated way by the newly developed CATCH-colonies software in the absence or presence of salinomycin.
    Results: Automated high-resolution colony formation analysis consistently identified the various colony types in a broad range of PCa cell lines. Serial clonogenic assays confirmed that holoclones show the highest colony formation potential and maintain their tumor-initiating capacity over multiple rounds. Furthermore, holoclones showed high expression of CD44, while CD24 was not expressed in these clones, thus representing the well-described tumor-initiating CD24
    Conclusions: Taken together, we demonstrated that salinomycin specifically targets the tumor-initiating cell population in docetaxel-sensitive and docetaxel-resistant PCa cells and may represent a potential therapeutic approach for the treatment of advanced PCa.
    MeSH term(s) Antineoplastic Combined Chemotherapy Protocols/pharmacology ; CD24 Antigen/biosynthesis ; Cell Line, Tumor ; Docetaxel/administration & dosage ; Docetaxel/pharmacology ; Drug Resistance, Neoplasm ; Humans ; Hyaluronan Receptors/biosynthesis ; Male ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; PC-3 Cells ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/pathology ; Pyrans/administration & dosage ; Pyrans/pharmacology
    Chemical Substances CD24 Antigen ; CD24 protein, human ; CD44 protein, human ; Hyaluronan Receptors ; Pyrans ; Docetaxel (15H5577CQD) ; salinomycin (62UXS86T64)
    Language English
    Publishing date 2019-12-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 604707-5
    ISSN 1097-0045 ; 0270-4137
    ISSN (online) 1097-0045
    ISSN 0270-4137
    DOI 10.1002/pros.23940
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1608: Show issues Location:
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  3. Article: Qualitäts- und Designkriterien für ein effizientes Kundenfeedbackinstrument am Praxisbeispiel einer Fluglinie

    Gruber, Martina

    Value Day 2012 : aktuelle Entwicklungen in Controlling, Finance & Strategy , p. 207-214

    2012  , Page(s) 207–214

    Author's details Martina Gruber
    Keywords Fluggesellschaft ; Beziehungsmarketing ; Kommunikation
    Language German
    Size graph. Darst.
    Publisher wvb, Wiss.-Verl.
    Publishing place Berlin
    Document type Article
    ISBN 978-3-86573-649-9 ; 3-86573-649-1
    Database ECONomics Information System

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  4. Article ; Online: Bactericidal and Fungicidal Activity of

    Gruber, Martina / Moser, Ivan / Nagl, Markus / Lackner, Michaela

    Antimicrobial agents and chemotherapy

    2017  Volume 61, Issue 5

    Abstract: Lung infections with multiresistant pathogens are a major problem among patients suffering from cystic fibrosis (CF). ...

    Abstract Lung infections with multiresistant pathogens are a major problem among patients suffering from cystic fibrosis (CF).
    MeSH term(s) Anti-Bacterial Agents/pharmacology ; Antifungal Agents/pharmacology ; Cystic Fibrosis/microbiology ; Escherichia coli/drug effects ; Fungi/drug effects ; Humans ; Lung Diseases, Fungal/drug therapy ; Lung Diseases, Fungal/microbiology ; Methicillin-Resistant Staphylococcus aureus/drug effects ; Microbial Sensitivity Tests ; Pseudomonas aeruginosa/drug effects ; Spores, Bacterial/drug effects ; Spores, Fungal/drug effects ; Sputum/microbiology ; Taurine/analogs & derivatives ; Taurine/pharmacology
    Chemical Substances Anti-Bacterial Agents ; Antifungal Agents ; Taurine (1EQV5MLY3D) ; N-chlorotaurine (51036-13-6)
    Language English
    Publishing date 2017-04-24
    Publishing country United States
    Document type Journal Article
    ZDB-ID 217602-6
    ISSN 1098-6596 ; 0066-4804
    ISSN (online) 1098-6596
    ISSN 0066-4804
    DOI 10.1128/AAC.02527-16
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Einzelsignatur: Show issues

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  5. Article ; Online: MYC-Mediated Ribosomal Gene Expression Sensitizes Enzalutamide-resistant Prostate Cancer Cells to EP300/CREBBP Inhibitors.

    Furlan, Tobias / Kirchmair, Alexander / Sampson, Natalie / Puhr, Martin / Gruber, Martina / Trajanoski, Zlatko / Santer, Frédéric R / Parson, Walther / Handle, Florian / Culig, Zoran

    The American journal of pathology

    2021  Volume 191, Issue 6, Page(s) 1094–1107

    Abstract: Patients with advanced prostate cancer are frequently treated with the antiandrogen enzalutamide. However, resistance eventually develops in virtually all patients, and various mechanisms have been associated with this process. The histone ... ...

    Abstract Patients with advanced prostate cancer are frequently treated with the antiandrogen enzalutamide. However, resistance eventually develops in virtually all patients, and various mechanisms have been associated with this process. The histone acetyltransferases EP300 and CREBBP are involved in regulation of cellular events in advanced prostate cancer. This study investigated the role of EP300/CREBBP inhibitors in enzalutamide-resistant prostate cancer. EP300/CREBBP inhibitors led to the same inhibition of androgen receptor activity in enzalutamide-resistant and -sensitive cells. However, enzalutamide-resistant cells were more sensitive to these inhibitors in viability assays. As indicated by the RNA-sequencing-based pathway analysis, genes related to the ribosome and MYC activity were significantly altered upon EP300/CREBBP inhibitor treatment. EP300/CREBBP inhibitors led to the down-regulation of ribosomal proteins RPL36 and RPL29. High-level ribosomal proteins amplifications and MYC amplifications were observed in castration-resistant prostate cancer samples of the publicly available Stand Up to Cancer data set. An inhibitor of RNA polymerase I-mediated transcription was used to evaluate the functional implications of these findings. The enzalutamide-resistant cell lines were more sensitive to this treatment. In addition, the migration rate of enzalutamide-resistant cells was strongly inhibited by this treatment. Taken together, the current data show that EP300/CREBBP inhibitors affect the MYC/ribosomal protein axis in enzalutamide-resistant cells and may have promising therapeutic implications.
    MeSH term(s) Androgen Antagonists ; Benzamides ; CREB-Binding Protein/metabolism ; Drug Resistance, Neoplasm/physiology ; E1A-Associated p300 Protein/metabolism ; Gene Expression Regulation, Neoplastic/physiology ; Humans ; Male ; Nitriles ; Phenylthiohydantoin ; Prostatic Neoplasms, Castration-Resistant/metabolism ; Proto-Oncogene Proteins c-myc/metabolism ; Ribosomal Proteins/metabolism
    Chemical Substances Androgen Antagonists ; Benzamides ; MYC protein, human ; Nitriles ; Proto-Oncogene Proteins c-myc ; Ribosomal Proteins ; Phenylthiohydantoin (2010-15-3) ; enzalutamide (93T0T9GKNU) ; CREB-Binding Protein (EC 2.3.1.48) ; CREBBP protein, human (EC 2.3.1.48) ; E1A-Associated p300 Protein (EC 2.3.1.48) ; EP300 protein, human (EC 2.3.1.48)
    Language English
    Publishing date 2021-03-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2943-9
    ISSN 1525-2191 ; 0002-9440
    ISSN (online) 1525-2191
    ISSN 0002-9440
    DOI 10.1016/j.ajpath.2021.02.017
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ud II Zs.76: Show issues Location:
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  6. Article ; Online: p300 is upregulated by docetaxel and is a target in chemoresistant prostate cancer.

    Gruber, Martina / Ferrone, Lavinia / Puhr, Martin / Santer, Frédéric R / Furlan, Tobias / Eder, Iris E / Sampson, Natalie / Schäfer, Georg / Handle, Florian / Culig, Zoran

    Endocrine-related cancer

    2020  Volume 27, Issue 3, Page(s) 187–198

    Abstract: Administration of the microtubule inhibitor docetaxel is a common treatment for metastatic castration-resistant prostate cancer (mCRPC) and results in prolonged patient overall survival. Usually, after a short period of time chemotherapy resistance ... ...

    Abstract Administration of the microtubule inhibitor docetaxel is a common treatment for metastatic castration-resistant prostate cancer (mCRPC) and results in prolonged patient overall survival. Usually, after a short period of time chemotherapy resistance emerges and there is urgent need to find new therapeutic targets to overcome therapy resistance. The lysine-acetyltransferase p300 has been correlated to prostate cancer (PCa) progression. Here, we aimed to clarify a possible function of p300 in chemotherapy resistance and verify p300 as a target in chemoresistant PCa. Immunohistochemistry staining of tissue samples revealed significantly higher p300 protein expression in patients who received docetaxel as a neoadjuvant therapy compared to control patients. Elevated p300 expression was confirmed by analysis of publicly available patient data, where significantly higher p300 mRNA expression was found in tissue of mCRPC tumors of docetaxel-treated patients. Consistently, docetaxel-resistant PCa cells showed increased p300 protein expression compared to docetaxel-sensitive counterparts. Docetaxel treatment of PCa cells for 72 h resulted in elevated p300 expression. shRNA-mediated p300 knockdown did not alter colony formation efficiency in docetaxel-sensitive cells, but significantly reduced clonogenic potential of docetaxel-resistant cells. Downregulation of p300 in docetaxel-resistant cells also impaired cell migration and invasion. Taken together, we showed that p300 is upregulated by docetaxel, and our findings suggest that p300 is a possible co-target in treatment of chemoresistant PCa.
    MeSH term(s) Cell Line, Tumor ; Cell Movement/drug effects ; Docetaxel/therapeutic use ; Drug Resistance, Neoplasm ; Humans ; Male ; Prostatic Neoplasms, Castration-Resistant/drug therapy ; Prostatic Neoplasms, Castration-Resistant/pathology ; Up-Regulation ; p300-CBP Transcription Factors/analysis ; p300-CBP Transcription Factors/antagonists & inhibitors ; p300-CBP Transcription Factors/genetics ; p300-CBP Transcription Factors/physiology
    Chemical Substances Docetaxel (15H5577CQD) ; p300-CBP Transcription Factors (EC 2.3.1.48) ; p300-CBP-associated factor (EC 2.3.1.48)
    Language English
    Publishing date 2020-01-17
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1218450-0
    ISSN 1479-6821 ; 1351-0088
    ISSN (online) 1479-6821
    ISSN 1351-0088
    DOI 10.1530/ERC-19-0488
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4192: Show issues Location:
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  7. Article ; Online: The STAT3 Inhibitor Galiellalactone Reduces IL6-Mediated AR Activity in Benign and Malignant Prostate Models.

    Handle, Florian / Puhr, Martin / Schaefer, Georg / Lorito, Nicla / Hoefer, Julia / Gruber, Martina / Guggenberger, Fabian / Santer, Frédéric R / Marques, Rute B / van Weerden, Wytske M / Claessens, Frank / Erb, Holger H H / Culig, Zoran

    Molecular cancer therapeutics

    2018  Volume 17, Issue 12, Page(s) 2722–2731

    Abstract: IL6/STAT3 signaling is associated with endocrine therapy resistance in prostate cancer, but therapies targeting this pathway in prostate cancer were unsuccessful in clinical trials so far. The mechanistic explanation for this phenomenon is currently ... ...

    Abstract IL6/STAT3 signaling is associated with endocrine therapy resistance in prostate cancer, but therapies targeting this pathway in prostate cancer were unsuccessful in clinical trials so far. The mechanistic explanation for this phenomenon is currently unclear; however, IL6 has pleiotropic effects on a number of signaling pathways, including the androgen receptor (AR). Therefore, we investigated IL6-mediated AR activation in prostate cancer cell lines and
    MeSH term(s) Androgens/pharmacology ; Animals ; Castration ; Cell Line, Tumor ; DNA/metabolism ; Humans ; Interleukin-6/pharmacology ; Lactones/pharmacology ; Male ; Mice, Nude ; Models, Biological ; Prostatic Neoplasms/pathology ; Protein Binding/drug effects ; Protein Domains ; Receptors, Androgen/metabolism ; STAT3 Transcription Factor/antagonists & inhibitors ; STAT3 Transcription Factor/chemistry ; STAT3 Transcription Factor/metabolism ; Signal Transduction/drug effects ; Xenograft Model Antitumor Assays
    Chemical Substances AR protein, human ; Androgens ; Interleukin-6 ; Lactones ; Receptors, Androgen ; STAT3 Transcription Factor ; galiellalactone ; DNA (9007-49-2)
    Language English
    Publishing date 2018-09-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2063563-1
    ISSN 1538-8514 ; 1535-7163
    ISSN (online) 1538-8514
    ISSN 1535-7163
    DOI 10.1158/1535-7163.MCT-18-0508
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5750: Show issues Location:
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