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  1. AU="Maymi, Valerie"
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  1. Article: Targeting of microRNA-22 Suppresses Tumor Spread in a Mouse Model of Triple-Negative Breast Cancer.

    Panella, Riccardo / Cotton, Cody A / Maymi, Valerie A / Best, Sachem / Berry, Kelsey E / Lee, Samuel / Batalini, Felipe / Vlachos, Ioannis S / Clohessy, John G / Kauppinen, Sakari / Pandolfi, Pier Paolo

    Biomedicines

    2023  Volume 11, Issue 5

    Abstract: microRNA-22 (miR-22) is an oncogenic miRNA whose up-regulation promotes epithelial-mesenchymal transition (EMT), tumor invasion, and metastasis in hormone-responsive breast cancer. Here we show that miR-22 plays a key role in triple negative breast ... ...

    Abstract microRNA-22 (miR-22) is an oncogenic miRNA whose up-regulation promotes epithelial-mesenchymal transition (EMT), tumor invasion, and metastasis in hormone-responsive breast cancer. Here we show that miR-22 plays a key role in triple negative breast cancer (TNBC) by promoting EMT and aggressiveness in 2D and 3D cell models and a mouse xenograft model of human TNBC, respectively. Furthermore, we report that miR-22 inhibition using an LNA-modified antimiR-22 compound is effective in reducing EMT both in vitro and in vivo. Importantly, pharmacologic inhibition of miR-22 suppressed metastatic spread and markedly prolonged survival in mouse xenograft models of metastatic TNBC highlighting the potential of miR-22 silencing as a new therapeutic strategy for the treatment of TNBC.
    Language English
    Publishing date 2023-05-18
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines11051470
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment.

    Maroni, Giorgia / Krishnan, Indira / Alfieri, Roberta / Maymi, Valerie A / Pandell, Nicole / Csizmadia, Eva / Zhang, Junyan / Weetall, Marla / Branstrom, Art / Braccini, Giulia / Cabrera San Millán, Eva / Storti, Barbara / Bizzarri, Ranieri / Kocher, Olivier / Daniela Sanchez Bassères, Daniela S / Welner, Robert S / Magli, Maria Cristina / Merelli, Ivan / Clohessy, John G /
    Ali, Azhar / Tenen, Daniel G / Levantini, Elena

    Cancer research communications

    2024  Volume 4, Issue 3, Page(s) 919–937

    Abstract: Lung cancer is the leading cause of cancer deaths. Lethal pulmonary adenocarcinomas (ADC) present with frequent mutations in the EGFR. Genetically engineered murine models of lung cancer expedited comprehension of the molecular mechanisms driving ... ...

    Abstract Lung cancer is the leading cause of cancer deaths. Lethal pulmonary adenocarcinomas (ADC) present with frequent mutations in the EGFR. Genetically engineered murine models of lung cancer expedited comprehension of the molecular mechanisms driving tumorigenesis and drug response. Here, we systematically analyzed the evolution of tumor heterogeneity in the context of dynamic interactions occurring with the intermingled tumor microenvironment (TME) by high-resolution transcriptomics. Our effort identified vulnerable tumor-specific epithelial cells, as well as their cross-talk with niche components (endothelial cells, fibroblasts, and tumor-infiltrating immune cells), whose symbiotic interface shapes tumor aggressiveness and is almost completely abolished by treatment with Unesbulin, a tubulin binding agent that reduces B cell-specific Moloney murine leukemia virus integration site 1 (BMI-1) activity. Simultaneous magnetic resonance imaging (MRI) analysis demonstrated decreased tumor growth, setting the stage for future investigations into the potential of novel therapeutic strategies for EGFR-mutant ADCs.
    Significance: Targeting the TME is an attractive strategy for treatment of solid tumors. Here we revealed how EGFR-mutant landscapes are affected at the single-cell resolution level during Unesbulin treatment. This novel drug, by targeting cancer cells and their interactions with crucial TME components, could be envisioned for future therapeutic advancements.
    MeSH term(s) Animals ; Mice ; Endothelial Cells ; Tumor Microenvironment/genetics ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Antineoplastic Agents ; Lung Neoplasms/drug therapy ; Cell Communication ; ErbB Receptors/genetics
    Chemical Substances Antineoplastic Agents ; ErbB Receptors (EC 2.7.10.1)
    Language English
    Publishing date 2024-03-28
    Publishing country United States
    Document type Journal Article
    ISSN 2767-9764
    ISSN (online) 2767-9764
    DOI 10.1158/2767-9764.CRC-23-0161
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: WWP1 inactivation enhances efficacy of PI3K inhibitors while suppressing their toxicities in breast cancer models.

    Kishikawa, Takahiro / Higuchi, Hiroshi / Wang, Limei / Panch, Nivedita / Maymi, Valerie / Best, Sachem / Lee, Samuel / Notoya, Genso / Toker, Alex / Matesic, Lydia E / Wulf, Gerburg M / Wei, Wenyi / Otsuka, Motoyuki / Koike, Kazuhiko / Clohessy, John G / Lee, Yu-Ru / Pandolfi, Pier Paolo

    The Journal of clinical investigation

    2021  Volume 131, Issue 24

    Abstract: Activation of the phosphatidylinositol 3-kinase (PI3K) signaling pathway is a pervasive event in tumorigenesis due to PI3K mutation and dysfunction of phosphatase and tensin homolog deleted on chromosome 10 (PTEN). Pharmacological inhibition of PI3K has ... ...

    Abstract Activation of the phosphatidylinositol 3-kinase (PI3K) signaling pathway is a pervasive event in tumorigenesis due to PI3K mutation and dysfunction of phosphatase and tensin homolog deleted on chromosome 10 (PTEN). Pharmacological inhibition of PI3K has resulted in variable clinical outcomes, however, raising questions regarding the possible mechanisms of unresponsiveness and resistance to treatment. WWP1 is an oncogenic HECT-type ubiquitin E3 ligase frequently amplified and mutated in multiple cancers, as well as in the germ lines of patients predisposed to cancer, and was recently found to activate PI3K signaling through PTEN inactivation. Here, we demonstrate that PTEN dissociated from the plasma membrane upon treatment with PI3K inhibitors through WWP1 activation, whereas WWP1 genetic or pharmacological inhibition restored PTEN membrane localization, synergizing with PI3K inhibitors to suppress tumor growth both in vitro and in vivo. Furthermore, we demonstrate that WWP1 inhibition attenuated hyperglycemia and the consequent insulin feedback, which is a major tumor-promoting side effect of PI3K inhibitors. Mechanistically, we found that AMPKα2 was ubiquitinated and, in turn, inhibited in its activatory phosphorylation by WWP1, whereas WWP1 inhibition facilitated AMPKα2 activity in the muscle to compensate for the reduction in glucose uptake observed upon PI3K inhibition. Thus, our identification of the cell-autonomous and systemic roles of WWP1 inhibition expands the therapeutic potential of PI3K inhibitors and reveals new avenues of combination cancer therapy.
    MeSH term(s) Animals ; Breast Neoplasms/drug therapy ; Breast Neoplasms/enzymology ; Breast Neoplasms/genetics ; Female ; Humans ; MCF-7 Cells ; Mammary Neoplasms, Experimental/drug therapy ; Mammary Neoplasms, Experimental/enzymology ; Mammary Neoplasms, Experimental/genetics ; Mice ; Mice, Knockout ; Mice, Nude ; Mice, SCID ; Neoplasm Proteins/antagonists & inhibitors ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphoinositide-3 Kinase Inhibitors/adverse effects ; Phosphoinositide-3 Kinase Inhibitors/pharmacology ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism
    Chemical Substances Neoplasm Proteins ; Phosphoinositide-3 Kinase Inhibitors ; WWP1 protein, human (EC 2.3.2.26) ; WWP1 protein, mouse (EC 2.3.2.26) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
    Language English
    Publishing date 2021-12-15
    Publishing country United States
    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.
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI140436
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ua VI Zs.184: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Identification of a targetable KRAS-mutant epithelial population in non-small cell lung cancer.

    Maroni, Giorgia / Bassal, Mahmoud A / Krishnan, Indira / Fhu, Chee Wai / Savova, Virginia / Zilionis, Rapolas / Maymi, Valerie A / Pandell, Nicole / Csizmadia, Eva / Zhang, Junyan / Storti, Barbara / Castaño, Julio / Panella, Riccardo / Li, Jia / Gustafson, Corinne E / Fox, Sam / Levy, Rachel D / Meyerovitz, Claire V / Tramontozzi, Peter J /
    Vermilya, Kimberly / De Rienzo, Assunta / Crucitta, Stefania / Bassères, Daniela S / Weetall, Marla / Branstrom, Art / Giorgetti, Alessandra / Ciampi, Raffaele / Del Re, Marzia / Danesi, Romano / Bizzarri, Ranieri / Yang, Henry / Kocher, Olivier / Klein, Allon M / Welner, Robert S / Bueno, Raphael / Magli, Maria Cristina / Clohessy, John G / Ali, Azhar / Tenen, Daniel G / Levantini, Elena

    Communications biology

    2021  Volume 4, Issue 1, Page(s) 370

    Abstract: Lung cancer is the leading cause of cancer deaths. Tumor heterogeneity, which hampers development of targeted therapies, was herein deconvoluted via single cell RNA sequencing in aggressive human adenocarcinomas (carrying Kras-mutations) and comparable ... ...

    Abstract Lung cancer is the leading cause of cancer deaths. Tumor heterogeneity, which hampers development of targeted therapies, was herein deconvoluted via single cell RNA sequencing in aggressive human adenocarcinomas (carrying Kras-mutations) and comparable murine model. We identified a tumor-specific, mutant-KRAS-associated subpopulation which is conserved in both human and murine lung cancer. We previously reported a key role for the oncogene BMI-1 in adenocarcinomas. We therefore investigated the effects of in vivo PTC596 treatment, which affects BMI-1 activity, in our murine model. Post-treatment, MRI analysis showed decreased tumor size, while single cell transcriptomics concomitantly detected near complete ablation of the mutant-KRAS-associated subpopulation, signifying the presence of a pharmacologically targetable, tumor-associated subpopulation. Our findings therefore hold promise for the development of a targeted therapy for KRAS-mutant adenocarcinomas.
    MeSH term(s) A549 Cells ; Animals ; Antineoplastic Agents ; Benzimidazoles/pharmacology ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/metabolism ; Carcinoma, Non-Small-Cell Lung/pathology ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; Molecular Targeted Therapy ; Mutation ; Polycomb Repressive Complex 1/genetics ; Polycomb Repressive Complex 1/metabolism ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins p21(ras)/genetics ; Pyrazines/pharmacology ; RNA-Seq ; Single-Cell Analysis ; Tumor Burden/drug effects ; Xenograft Model Antitumor Assays ; Mice
    Chemical Substances Antineoplastic Agents ; BMI1 protein, human ; Benzimidazoles ; Bmi1 protein, mouse ; KRAS protein, human ; PTC596 ; Proto-Oncogene Proteins ; Pyrazines ; Polycomb Repressive Complex 1 (EC 2.3.2.27) ; Hras protein, mouse (EC 3.6.5.2) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
    Language English
    Publishing date 2021-04-14
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2399-3642
    ISSN (online) 2399-3642
    DOI 10.1038/s42003-021-01897-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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