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  1. Article ; Online: miRNAs and Melanoma

    Adriana Taveira da Cruz / Miriam Galvonas Jasiulionis

    Dermatology Research and Practice, Vol

    How Are They Connected?

    2012  Volume 2012

    Keywords Dermatology ; RL1-803 ; Medicine ; R
    Language English
    Publishing date 2012-01-01T00:00:00Z
    Publisher Hindawi Publishing Corporation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: miR-138-5p induces aggressive traits by targeting Trp53 expression in murine melanoma cells, and correlates with poor prognosis of melanoma patients.

    da Cruz, Adriana Taveira / Hunger, Aline / de Melo, Fabiana Henriques Machado / Monteiro, Ana Carolina / Paré, Geneviève Catherine / Lai, Dulce / Alves-Fernandes, Débora Kristina / Ayub, Ana Luisa Pedroso / Cordero, Esteban Mauricio / Filho, José Franco da Silveira / Schneider-Stock, Regine / Strauss, Bryan Eric / Tron, Victor / Jasiulionis, Miriam Galvonas

    Neoplasia (New York, N.Y.)

    2021  Volume 23, Issue 8, Page(s) 823–834

    Abstract: Deregulation of miRNAs contributes to the development of distinct cancer types, including melanoma, an aggressive form of skin cancer characterized by high metastatic potential and poor prognosis. The expression of a set of 580 miRNAs was investigated in ...

    Abstract Deregulation of miRNAs contributes to the development of distinct cancer types, including melanoma, an aggressive form of skin cancer characterized by high metastatic potential and poor prognosis. The expression of a set of 580 miRNAs was investigated in a model of murine melanoma progression, comprising non-metastatic (4C11-) and metastatic melanoma (4C11+) cells. A significant increase in miR-138-5p expression was found in the metastatic 4C11+ melanoma cells compared to 4C11-, which prompted us to investigate its role in melanoma aggressiveness. Functional assays, including anoikis resistance, colony formation, collective migration, serum-deprived growth capacity, as well as in vivo tumor growth and experimental metastasis were performed in 4C11- cells stably overexpressing miR-138-5p. miR-138-5p induced an aggressive phenotype in mouse melanoma cell lines leading to increased proliferation, migration and cell viability under stress conditions. Moreover, by overexpressing miR-138-5p, low-growing and non-metastatic 4C11- cells became highly proliferative and metastatic in vivo, similar to the metastatic 4C11+ cells. Luciferase reporter analysis identified the tumor suppressor Trp53 as a direct target of miR-138-5p. Using data sets from independent melanoma cohorts, miR-138-5p and P53 expression were also found deregulated in human melanoma samples, with their levels negatively and positively correlated with prognosis, respectively. Our data shows that the overexpression of miR-138-5p contributes to melanoma metastasis through the direct suppression of Trp53.
    MeSH term(s) 3' Untranslated Regions ; Animals ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Humans ; Melanoma/genetics ; Melanoma/mortality ; Melanoma/pathology ; Mice ; MicroRNAs/genetics ; Neoplasm Metastasis ; Neoplasm Staging ; Prognosis ; RNA Interference ; Survival Analysis ; Tumor Suppressor Protein p53/genetics
    Chemical Substances 3' Untranslated Regions ; MIRN138 microRNA, human ; MIRN138 microRNA, mouse ; MicroRNAs ; Trp53 protein, mouse ; Tumor Suppressor Protein p53
    Language English
    Publishing date 2021-07-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1483840-0
    ISSN 1476-5586 ; 1522-8002
    ISSN (online) 1476-5586
    ISSN 1522-8002
    DOI 10.1016/j.neo.2021.05.015
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5203: 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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  3. Article ; Online: miRNAs and Melanoma: How Are They Connected?

    da Cruz, Adriana Taveira / Jasiulionis, Miriam Galvonas

    Dermatology research and practice

    2011  Volume 2012, Page(s) 528345

    Abstract: miRNAs are non-coding RNAs that bind to mRNA targets and disturb their stability and/or translation, thus acting in gene posttranscriptional regulation. It is predicted that over 30% of mRNAs are regulated by miRNAs. Therefore these molecules are ... ...

    Abstract miRNAs are non-coding RNAs that bind to mRNA targets and disturb their stability and/or translation, thus acting in gene posttranscriptional regulation. It is predicted that over 30% of mRNAs are regulated by miRNAs. Therefore these molecules are considered essential in the processing of many biological responses, such as cell proliferation, apoptosis, and stress responsiveness. As miRNAs participate of virtually all cellular pathways, their deregulation is critical to cancer development. Consequently, loss or gain of miRNAs function may contribute to tumor progression. Little is known about the regulation of miRNAs and understanding the events that lead to changes in their expression may provide new perspectives for cancer treatment. Among distinct types of cancer, melanoma has special implications. It is characterized as a complex disease, originated from a malignant transformation of melanocytes. Despite being rare, its metastatic form is usually incurable, which makes melanoma the major death cause of all skin cancers. Some molecular pathways are frequently disrupted in melanoma, and miRNAs probably have a decisive role on these alterations. Therefore, this review aims to discuss new findings about miRNAs in melanoma fields, underlying epigenetic processes, and also to argue possibilities of using miRNAs in melanoma diagnosis and therapy.
    Language English
    Publishing date 2011-08-10
    Publishing country Egypt
    Document type Journal Article
    ZDB-ID 2548952-5
    ISSN 1687-6113 ; 1687-6105
    ISSN (online) 1687-6113
    ISSN 1687-6105
    DOI 10.1155/2012/528345
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: α- L-iduronidase gene-based therapy using the phiC31 system to treat mucopolysaccharidose type I mice.

    Stilhano, Roberta Sessa / Martin, Priscila Keiko Matsumoto / de Melo, Suely Maymone / Samoto, Vivian Yochiko / Peres, Giovani Bravin / da Silva Michelacci, Yara Maria Correa / da Silva, Flavia Helena / Pereira, Vanessa Gonçalves / D'Almeida, Vania / da Cruz, Adriana Taveira / Jasiulionis, Miriam Galvonas / Han, Sang Won

    The journal of gene medicine

    2015  Volume 17, Issue 1-2, Page(s) 1–13

    Abstract: Background: Mucopolysaccharidose type I (MPSI) is a lysosomal monogenic disease caused by mutations in the gene for α- L-iduronidase (IDUA). MPSI patients need a constant supply of IDUA to alleviate progression of the disease. IDUA gene transfer using ... ...

    Abstract Background: Mucopolysaccharidose type I (MPSI) is a lysosomal monogenic disease caused by mutations in the gene for α- L-iduronidase (IDUA). MPSI patients need a constant supply of IDUA to alleviate progression of the disease. IDUA gene transfer using integrative vectors might provide a definitive solution and support advancement to clinical trials, although studies have not yet been satisfactory. To achieve a stable IDUA gene expression in vivo, phiC31 was tested in the present study.
    Methods: Several plasmid vectors were constructed and IDUA-/- mice were treated with cyclophosphamide and transfected with these vectors hydrodynamically via tail veins. IDUA expression was monitored over time. Treated and nontreated mice underwent an open-field test at age 8 months, and IDUA activity and glycosaminoglycan (GAG) content of tissues were evaluated.
    Results: High levels of IDUA activity were detected initially (>1000 U/ml), although these levels decayed over time. The reinjection of vectors produced a similar profile of IDUA decay. Three out of six treated mice had IDUA activity in the livers, and also showed lower GAG content, reduced lysosomes and better locomotion. To investigate unsustained IDUA production, wild-type mice were submitted to the same gene therapy procedure, which generated a similar profile of IDUA decay. Anti-IDUA antibody was detected in the sera of these animals. In addition, we also found three methylated sites in the cytomegalovirus promoter region.
    Conclusions: phiC31-mediated gene therapy resulted in an important improvement in IDUA-/- mice, including locomotion, although the obstacles that need to be overcome to enable long-term gene therapy for MPSI are also noted.
    MeSH term(s) Animals ; Behavior, Animal ; Cell Line ; DNA Methylation ; Disease Models, Animal ; Enzyme Activation ; Female ; Gene Expression ; Gene Order ; Gene Transfer Techniques ; Genes, Reporter ; Genetic Therapy ; Genetic Vectors/administration & dosage ; Genetic Vectors/genetics ; HEK293 Cells ; Homologous Recombination ; Humans ; Iduronidase/genetics ; Iduronidase/metabolism ; Liver/metabolism ; Liver/pathology ; Male ; Mice ; Mice, Knockout ; Motor Activity ; Mucopolysaccharidosis I/genetics ; Mucopolysaccharidosis I/metabolism ; Mucopolysaccharidosis I/therapy ; Nucleotide Motifs ; Promoter Regions, Genetic ; Transfection
    Chemical Substances Iduronidase (EC 3.2.1.76)
    Language English
    Publishing date 2015-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1458024-x
    ISSN 1521-2254 ; 1099-498X
    ISSN (online) 1521-2254
    ISSN 1099-498X
    DOI 10.1002/jgm.2818
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5423: 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)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

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