Oncogenic Potential of the miR-106-363 Cluster and Its Implication in Human T-Cell Leukemia. Export

@article{citeulike:1399498, abstract = {We previously reported the identification of the Kis2 common retrovirus integration site, located on mouse chromosome X, in radiation leukemia virus-induced T-cell leukemias. Tumors with a provirus at the Kis2 locus overexpressed a novel noncoding RNA (ncRNA) with a complex splicing pattern and no polyA tail. Database upgrade revealed the presence of a microRNA (miRNA) cluster, miR-106-363, just downstream of the Kis2 ncRNAs. We found that Kis2 ncRNAs are the pri-miRNA of miR-106-363, and we present evidence that Kis2 ncRNA overexpression in mouse tumors results in miR-106a, miR-19b-2, miR-92-2, and miR-20b accumulation. We show the oncogenic potential of those miRNAs in anchorage independence assay and confirm pri-miR-106-363 overexpression in 46\% of human T-cell leukemias tested. This overexpression contributes in rising miR-92 and miR-19 levels, as this is the case for miR-17-92 cluster overexpression. Furthermore, we identified myosin regulatory light chain-interacting protein, retinoblastoma-binding protein 1-like, and possibly homeodomain-interacting protein kinase 3 as target genes of this miRNA cluster, which establishes a link between these genes and T-cell leukemia for the first time. [Cancer Res 2007;67(12):5699-707].}, address = {Laboratoire de Biologie Mol\'{e}culaire, D\'{e}partement des Sciences Biologiques, Universit\'{e} du Qu\'{e}bec \`{a} Montr\'{e}al, Montreal, Quebec, Canada.}, author = {Landais, S. and Landry, S. and Legault, P. and Rassart, E.}, citeulike-article-id = {1399498}, citeulike-linkout-0 = {http://dx.doi.org/10.1158/0008-5472.CAN-06-4478}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/17575136}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=17575136}, day = {15}, doi = {10.1158/0008-5472.CAN-06-4478}, issn = {0008-5472}, journal = {Cancer Res}, keywords = {cluster, disorder, mirna, ncrna}, month = {June}, number = {12}, pages = {5699--5707}, posted-at = {2007-06-20 02:52:34}, priority = {0}, title = {Oncogenic Potential of the miR-106-363 Cluster and Its Implication in Human T-Cell Leukemia.}, url = {http://dx.doi.org/10.1158/0008-5472.CAN-06-4478}, volume = {67}, year = {2007} }

TY - JOUR ID - citeulike:1399498 L3 - citeulike-article-id:1399498 N2 - We previously reported the identification of the Kis2 common retrovirus integration site, located on mouse chromosome X, in radiation leukemia virus-induced T-cell leukemias. Tumors with a provirus at the Kis2 locus overexpressed a novel noncoding RNA (ncRNA) with a complex splicing pattern and no polyA tail. Database upgrade revealed the presence of a microRNA (miRNA) cluster, miR-106-363, just downstream of the Kis2 ncRNAs. We found that Kis2 ncRNAs are the pri-miRNA of miR-106-363, and we present evidence that Kis2 ncRNA overexpression in mouse tumors results in miR-106a, miR-19b-2, miR-92-2, and miR-20b accumulation. We show the oncogenic potential of those miRNAs in anchorage independence assay and confirm pri-miR-106-363 overexpression in 46% of human T-cell leukemias tested. This overexpression contributes in rising miR-92 and miR-19 levels, as this is the case for miR-17-92 cluster overexpression. Furthermore, we identified myosin regulatory light chain-interacting protein, retinoblastoma-binding protein 1-like, and possibly homeodomain-interacting protein kinase 3 as target genes of this miRNA cluster, which establishes a link between these genes and T-cell leukemia for the first time. [Cancer Res 2007;67(12):5699-707]. IS - 12 JF - Cancer Res SN - 0008-5472 AD - Laboratoire de Biologie Moléculaire, Département des Sciences Biologiques, Université du Québec à Montréal, Montreal, Quebec, Canada. EP - 5707 TI - Oncogenic Potential of the miR-106-363 Cluster and Its Implication in Human T-Cell Leukemia. VL - 67 SP - 5699 KW - cluster KW - disorder KW - mirna KW - ncrna AU - Landais, S AU - Landry, S AU - Legault, P AU - Rassart, E PY - 2007/06/15/ UR - http://dx.doi.org/10.1158/0008-5472.CAN-06-4478 ER -