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  1. Article: A role for miR-34 in colon cancer stem cell homeostasis.

    Rupaimoole, Rajesha / Slack, Frank J

    Stem cell investigation

    2016  Volume 3, Page(s) 42

    Language English
    Publishing date 2016-08-24
    Publishing country China
    Document type Comment ; Editorial
    ZDB-ID 2884645-X
    ISSN 2313-0792 ; 2306-9759
    ISSN (online) 2313-0792
    ISSN 2306-9759
    DOI 10.21037/sci.2016.08.04
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  2. Article ; Online: MicroRNA therapeutics: towards a new era for the management of cancer and other diseases.

    Rupaimoole, Rajesha / Slack, Frank J

    Nature reviews. Drug discovery

    2017  Volume 16, Issue 3, Page(s) 203–222

    Abstract: In just over two decades since the discovery of the first microRNA (miRNA), the field of miRNA biology has expanded considerably. Insights into the roles of miRNAs in development and disease, particularly in cancer, have made miRNAs attractive tools and ... ...

    Abstract In just over two decades since the discovery of the first microRNA (miRNA), the field of miRNA biology has expanded considerably. Insights into the roles of miRNAs in development and disease, particularly in cancer, have made miRNAs attractive tools and targets for novel therapeutic approaches. Functional studies have confirmed that miRNA dysregulation is causal in many cases of cancer, with miRNAs acting as tumour suppressors or oncogenes (oncomiRs), and miRNA mimics and molecules targeted at miRNAs (antimiRs) have shown promise in preclinical development. Several miRNA-targeted therapeutics have reached clinical development, including a mimic of the tumour suppressor miRNA miR-34, which reached phase I clinical trials for treating cancer, and antimiRs targeted at miR-122, which reached phase II trials for treating hepatitis. In this article, we describe recent advances in our understanding of miRNAs in cancer and in other diseases and provide an overview of current miRNA therapeutics in the clinic. We also discuss the challenge of identifying the most efficacious therapeutic candidates and provide a perspective on achieving safe and targeted delivery of miRNA therapeutics.
    MeSH term(s) Animals ; Clinical Trials as Topic/methods ; Disease Management ; Genetic Therapy/methods ; Genetic Therapy/trends ; Humans ; MicroRNAs/administration & dosage ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/therapy
    Chemical Substances MicroRNAs
    Language English
    Publishing date 2017-03
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2062954-0
    ISSN 1474-1784 ; 1474-1776
    ISSN (online) 1474-1784
    ISSN 1474-1776
    DOI 10.1038/nrd.2016.246
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5564: Show issues Location:
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    Zs.MO 334: Show issues
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  3. Article ; Online: A High-Throughput Small Molecule Screen Identifies Ouabain as Synergistic with miR-34a in Killing Lung Cancer Cells.

    Rupaimoole, Rajesha / Yoon, Bohyung / Zhang, Wen Cai / Adams, Brian D / Slack, Frank J

    iScience

    2020  Volume 23, Issue 2, Page(s) 100878

    Abstract: MicroRNA-34 (miR-34) is one of the major families of tumor suppressor miRNAs often lost in cancers. Delivery of miR-34a mimics to affected tumors as a therapeutic strategy has been tried in pre-clinical studies and in a phase I clinical trial. One ... ...

    Abstract MicroRNA-34 (miR-34) is one of the major families of tumor suppressor miRNAs often lost in cancers. Delivery of miR-34a mimics to affected tumors as a therapeutic strategy has been tried in pre-clinical studies and in a phase I clinical trial. One approach to increase efficacy and reduce toxicity is to rationally identify drug combinations with small molecules that synergize with miR-34a. In this study we performed a high-throughput screen of a large panel of small molecules with known biological activity and identified ouabain as a candidate small molecule that synergized with miR-34a in killing lung cancer cells. We elucidated autophagy activation as a key mechanism by which miR-34a and ouabain causes increased cytotoxicity in cells. We posit that this combinatorial approach could reduce the active dose of miR-34a needed in vivo to observe tumor shrinkage and potentiate the development of miR-34a combination therapies in the future.
    Language English
    Publishing date 2020-02-01
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2020.100878
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  4. Article ; Online: A High-Throughput Small Molecule Screen Identifies Ouabain as Synergistic with miR-34a in Killing Lung Cancer Cells

    Rajesha Rupaimoole / Bohyung Yoon / Wen Cai Zhang / Brian D. Adams / Frank J. Slack

    iScience, Vol 23, Iss 2, Pp - (2020)

    2020  

    Abstract: Summary: MicroRNA-34 (miR-34) is one of the major families of tumor suppressor miRNAs often lost in cancers. Delivery of miR-34a mimics to affected tumors as a therapeutic strategy has been tried in pre-clinical studies and in a phase I clinical trial. ... ...

    Abstract Summary: MicroRNA-34 (miR-34) is one of the major families of tumor suppressor miRNAs often lost in cancers. Delivery of miR-34a mimics to affected tumors as a therapeutic strategy has been tried in pre-clinical studies and in a phase I clinical trial. One approach to increase efficacy and reduce toxicity is to rationally identify drug combinations with small molecules that synergize with miR-34a. In this study we performed a high-throughput screen of a large panel of small molecules with known biological activity and identified ouabain as a candidate small molecule that synergized with miR-34a in killing lung cancer cells. We elucidated autophagy activation as a key mechanism by which miR-34a and ouabain causes increased cytotoxicity in cells. We posit that this combinatorial approach could reduce the active dose of miR-34a needed in vivo to observe tumor shrinkage and potentiate the development of miR-34a combination therapies in the future. : Biomolecules; Biotechnology; Cancer Subject Areas: Biomolecules, Biotechnology, Cancer
    Keywords Science ; Q
    Subject code 610 ; 500
    Language English
    Publishing date 2020-02-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: miRNA Deregulation in Cancer Cells and the Tumor Microenvironment.

    Rupaimoole, Rajesha / Calin, George A / Lopez-Berestein, Gabriel / Sood, Anil K

    Cancer discovery

    2016  Volume 6, Issue 3, Page(s) 235–246

    Abstract: Unlabelled: miRNAs are a key component of the noncoding RNA family. The underlying mechanisms involved in the interplay between the tumor microenvironment and cancer cells involve highly dynamic factors such as hypoxia and cell types such as cancer- ... ...

    Abstract Unlabelled: miRNAs are a key component of the noncoding RNA family. The underlying mechanisms involved in the interplay between the tumor microenvironment and cancer cells involve highly dynamic factors such as hypoxia and cell types such as cancer-associated fibroblasts and macrophages. Although miRNA levels are known to be altered in cancer cells, recent evidence suggests a critical role for the tumor microenvironment in regulating miRNA biogenesis, methylation, and transcriptional changes. Here, we discuss the complex protumorigenic symbiotic role between tumor cells, the tumor microenvironment, and miRNA deregulation.
    Significance: miRNAs play a central role in cell signaling and homeostasis. In this article, we provide insights into the regulatory mechanisms involved in the deregulation of miRNAs in cancer cells and the tumor microenvironment and discuss therapeutic intervention strategies to overcome this deregulation.
    MeSH term(s) Animals ; Cell Transformation, Neoplastic/genetics ; Disease Progression ; Fibroblasts/metabolism ; Gene Expression Regulation, Neoplastic ; Gene Regulatory Networks ; Humans ; Hypoxia/genetics ; Hypoxia/metabolism ; Inflammation/etiology ; Inflammation/metabolism ; Inflammation/pathology ; MicroRNAs/genetics ; MicroRNAs/therapeutic use ; Neoplasms/genetics ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/pathology ; Signal Transduction ; Tumor Microenvironment/genetics
    Chemical Substances MicroRNAs
    Language English
    Publishing date 2016-03
    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. ; Review
    ZDB-ID 2625242-9
    ISSN 2159-8290 ; 2159-8274
    ISSN (online) 2159-8290
    ISSN 2159-8274
    DOI 10.1158/2159-8290.CD-15-0893
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6916: Show issues Location:
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  6. Article: Macrophage TGF-

    Moritz, Robert J / LeBaron, Richard G / Phelix, Clyde F / Rupaimoole, Rajesha / Kim, Hong Seok / Tsin, Andrew / Asmis, Reto

    International journal of clinical medicine

    2016  Volume 7, Issue 7, Page(s) 496–510

    Abstract: Metabolically stressed kidney is in part characterized by infiltrating macrophages and macrophage-derived TGF- ...

    Abstract Metabolically stressed kidney is in part characterized by infiltrating macrophages and macrophage-derived TGF-
    Language English
    Publishing date 2016-07-21
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2604663-5
    ISSN 2158-2882 ; 2158-284X
    ISSN (online) 2158-2882
    ISSN 2158-284X
    DOI 10.4236/ijcm.2016.77055
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  7. Article ; Online: Personalized RNA Medicine for Pancreatic Cancer.

    Gilles, Maud-Emmanuelle / Hao, Liangliang / Huang, Ling / Rupaimoole, Rajesha / Lopez-Casas, Pedro P / Pulver, Emilia / Jeong, Jong Cheol / Muthuswamy, Senthil K / Hidalgo, Manuel / Bhatia, Sangeeta N / Slack, Frank J

    Clinical cancer research : an official journal of the American Association for Cancer Research

    2018  Volume 24, Issue 7, Page(s) 1734–1747

    Abstract: Purpose: ...

    Abstract Purpose:
    MeSH term(s) Animals ; Carcinoma, Pancreatic Ductal/genetics ; Cell Line, Tumor ; Cell Proliferation/genetics ; Disease Models, Animal ; Gene Expression Profiling/methods ; Humans ; Mice ; Mice, Nude ; MicroRNAs/genetics ; Oncogenes/genetics ; Pancreatic Neoplasms/genetics ; Precision Medicine/methods ; Xenograft Model Antitumor Assays/methods ; Pancreatic Neoplasms
    Chemical Substances MicroRNAs
    Language English
    Publishing date 2018-01-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-17-2733
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4223: Show issues Location:
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  8. Article ; Online: Pan-cancer genomic analysis links 3'UTR DNA methylation with increased gene expression in T cells.

    McGuire, Michael H / Herbrich, Shelley M / Dasari, Santosh K / Wu, Sherry Y / Wang, Ying / Rupaimoole, Rajesha / Lopez-Berestein, Gabriel / Baggerly, Keith A / Sood, Anil K

    EBioMedicine

    2019  Volume 43, Page(s) 127–137

    Abstract: Background: Investigations into the function of non-promoter DNA methylation have yielded new insights into the epigenetic regulation of gene expression. However, integrated genome-wide non-promoter DNA methylation and gene expression analyses across a ... ...

    Abstract Background: Investigations into the function of non-promoter DNA methylation have yielded new insights into the epigenetic regulation of gene expression. However, integrated genome-wide non-promoter DNA methylation and gene expression analyses across a wide number of tumour types and corresponding normal tissues have not been performed.
    Methods: To investigate the impact of non-promoter DNA methylation on cancer pathogenesis, we performed a large-scale analysis of gene expression and DNA methylation profiles, finding enrichment in the 3'UTR DNA methylation positively correlated with gene expression. Filtering for genes in which 3'UTR DNA methylation strongly correlated with gene expression yielded a list of genes enriched for functions involving T cell activation.
    Findings: The important immune checkpoint gene Havcr2 showed a substantial increase in 3'UTR DNA methylation upon T cell activation and subsequent upregulation of gene expression in mice. Furthermore, this increase in Havcr2 gene expression was abrogated by treatment with decitabine.
    Interpretation: These findings indicate that the 3'UTR is a functionally relevant DNA methylation site. Additionally, we show a potential novel mechanism of HAVCR2 regulation in T cells, providing new insights for modulating immune checkpoint blockade.
    MeSH term(s) 3' Untranslated Regions ; Animals ; Biomarkers, Tumor ; Computational Biology/methods ; DNA (Cytosine-5-)-Methyltransferases/genetics ; DNA Methylation ; Databases, Genetic ; Epigenesis, Genetic ; Female ; Flow Cytometry ; Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Genomics/methods ; Hepatitis A Virus Cellular Receptor 2/genetics ; Humans ; Lymphocyte Activation/immunology ; Mice ; Neoplasms/genetics ; Neoplasms/immunology ; Neoplasms/mortality ; Prognosis ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism
    Chemical Substances 3' Untranslated Regions ; Biomarkers, Tumor ; HAVCR2 protein, human ; Hepatitis A Virus Cellular Receptor 2 ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37) ; DNA methyltransferase 3A (EC 2.1.1.37)
    Language English
    Publishing date 2019-05-02
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2851331-9
    ISSN 2352-3964
    ISSN (online) 2352-3964
    DOI 10.1016/j.ebiom.2019.04.045
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    Zs.A 7090: Show issues Location:
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  9. Article ; Online: ATP11B mediates platinum resistance in ovarian cancer.

    Moreno-Smith, Myrthala / Halder, J B / Meltzer, Paul S / Gonda, Tamas A / Mangala, Lingegowda S / Rupaimoole, Rajesha / Lu, Chunhua / Nagaraja, Archana S / Gharpure, Kshipra M / Kang, Yu / Rodriguez-Aguayo, Cristian / Vivas-Mejia, Pablo E / Zand, Behrouz / Schmandt, Rosemarie / Wang, Hua / Langley, Robert R / Jennings, Nicholas B / Ivan, Cristina / Coffin, Jeremy E /
    Armaiz, Guillermo N / Bottsford-Miller, Justin / Kim, Sang Bae / Halleck, Margaret S / Hendrix, Mary Jc / Bornman, William / Bar-Eli, Menashe / Lee, Ju-Seog / Siddik, Zahid H / Lopez-Berestein, Gabriel / Sood, Anil K

    The Journal of clinical investigation

    2021  Volume 131, Issue 7

    Language English
    Publishing date 2021-04-01
    Publishing country United States
    Document type Journal Article ; Published Erratum
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI149893
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  10. Article ; Online: Improving vascular maturation using noncoding RNAs increases antitumor effect of chemotherapy.

    Mangala, Lingegowda S / Wang, Hongyu / Jiang, Dahai / Wu, Sherry Y / Somasunderam, Anoma / Volk, David E / Lokesh, Ganesh L R / Li, Xin / Pradeep, Sunila / Yang, Xianbin / Haemmerle, Monika / Rodriguez-Aguayo, Cristian / Nagaraja, Archana S / Rupaimoole, Rajesha / Bayraktar, Emine / Bayraktar, Recep / Li, Li / Tanaka, Takemi / Hu, Wei /
    Ivan, Cristina / Gharpure, Kshipra M / McGuire, Michael H / Thiviyanathan, Varatharasa / Zhang, Xinna / Maiti, Sourindra N / Bulayeva, Nataliya / Choi, Hyun-Jin / Dorniak, Piotr L / Cooper, Laurence Jn / Rosenblatt, Kevin P / Lopez-Berestein, Gabriel / Gorenstein, David G / Sood, Anil K

    JCI insight

    2021  Volume 6, Issue 7

    Language English
    Publishing date 2021-04-08
    Publishing country United States
    Document type Journal Article ; Published Erratum
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.149896
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