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pubmed, cancer, article, cells, google, scholar, cas, pancreatic, cell, stem, population, microrna, central, zhao, human, side, tumor, wang, expression, research, munich, lplgressp, access, res, liu, tumors, resistance, bao, renner, bruns, celllike, metastatic, mirna, invasion, primary, targeting, rev, nat, oncol, privacy, cookies, content, stemlike, metastasis, jauch, peter, camaj, significant, antagomir, proliferation,

Topics {✒️}

month download article/chapter hypoxia-inducible factor-1alpha expression tgf-beta-mediated epithelial abc transporter bcrp1/abcg2 karl-walter jauch mir-21-mediated tumor growth cells modulates tumorigenesis proapoptotic genes mapk10/jnk3 otto-von-guericke university full article pdf related subjects microrna-200b reverses chemoresistance metastatic pancreatic cancer 6plgres-sp cells demonstrating human pancreatic adenocarcinoma advanced pancreatic carcinoma cancer stem cell pancreatic cancer cells cancer stem cells privacy choices/manage cookies human glioblastoma cells side-population phenotype highly significant difference human gastrointestinal system metastatic lesions generated primary tumors generated embryonic stem cells stepwise metastatic potentials föfole research program german research society tumor-initiating stem pancreatic cyst fluid posttranscriptional gene silencing side population cells cell population compared sp cell fraction side population purified side population derived cell cycle progression microrna expression signature transcriptional repression mediated multiple drug resistance underwent radical surgery mirna-221 antisense oligonucleotides aggressive tumor formation mirnas vivo tumor growth mir-222 expression affects sorted sp cells 6pl cell proliferation

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         headline:Antisense inhibition of microRNA-21 and microRNA-221 in tumor-initiating stem-like cells modulates tumorigenesis, metastasis, and chemotherapy resistance in pancreatic cancer
         description:Our preliminary studies identified a small population side population (SP) cells in pancreatic cancer cells with stem cell-like properties, which were able to induce fast and aggressive tumor formation in nude mice. Gene expression analysis showed a significant difference in the expression of more than 1,300 genes in SP cells, among which a highly significant difference in microRNA expression of miR-21 and miR-221 between SP and NSP cells was identified. SP cells were identified and characterized by flow cytometry using Hoechst 33342 dye staining from a highly metastatic human pancreatic cancer cell line (L3.6pl). Antagomir transfection was performed using miRNA-21 and miRNA-221 antisense oligonucleotides (ASOs) and followed by detection of cell apoptosis, cell cycle progression, chemosensitivity, and invasion. Sorted SP cells from gemcitabine-resistant L3.6pl cells (L3.6plGres-SP) cells were orthotopically implanted in nude mice with or without miRNA-21 and miRNA-221 ASOs mono- and combination therapy. The administration of antagomir-21 and antagomir-221 significantly reduced the SP cell fraction, decreased SP cell differentiation, and downstream gene regulation, and thereby induced reduction of L3.6pl cell proliferation, invasion, and chemoresistance against gemcitabine and 5-Fluorouracil. Combination of ASOs therapy against miRNA-21 and miRNA-221 significantly inhibited primary tumor growth and metastasis compared to single antagomir treatment, especially, in L3.6plGres-SP-induced pancreatic tumor growth in vivo. These findings further indicate that the inhibition of miR-21 and miR-221 appear particularly suitable to target stem-like subpopulations and address their specific biological function to promote tumor progression in pancreatic cancer.
         datePublished:2015-02-03T00:00:00Z
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            miRNAs
            Side population
            Tumorigenesis
            Metastasis
            Chemotherapy resistance
            Pancreatic cancer
            Oncology
            Biomedicine
            general
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      headline:Antisense inhibition of microRNA-21 and microRNA-221 in tumor-initiating stem-like cells modulates tumorigenesis, metastasis, and chemotherapy resistance in pancreatic cancer
      description:Our preliminary studies identified a small population side population (SP) cells in pancreatic cancer cells with stem cell-like properties, which were able to induce fast and aggressive tumor formation in nude mice. Gene expression analysis showed a significant difference in the expression of more than 1,300 genes in SP cells, among which a highly significant difference in microRNA expression of miR-21 and miR-221 between SP and NSP cells was identified. SP cells were identified and characterized by flow cytometry using Hoechst 33342 dye staining from a highly metastatic human pancreatic cancer cell line (L3.6pl). Antagomir transfection was performed using miRNA-21 and miRNA-221 antisense oligonucleotides (ASOs) and followed by detection of cell apoptosis, cell cycle progression, chemosensitivity, and invasion. Sorted SP cells from gemcitabine-resistant L3.6pl cells (L3.6plGres-SP) cells were orthotopically implanted in nude mice with or without miRNA-21 and miRNA-221 ASOs mono- and combination therapy. The administration of antagomir-21 and antagomir-221 significantly reduced the SP cell fraction, decreased SP cell differentiation, and downstream gene regulation, and thereby induced reduction of L3.6pl cell proliferation, invasion, and chemoresistance against gemcitabine and 5-Fluorouracil. Combination of ASOs therapy against miRNA-21 and miRNA-221 significantly inhibited primary tumor growth and metastasis compared to single antagomir treatment, especially, in L3.6plGres-SP-induced pancreatic tumor growth in vivo. These findings further indicate that the inhibition of miR-21 and miR-221 appear particularly suitable to target stem-like subpopulations and address their specific biological function to promote tumor progression in pancreatic cancer.
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         miRNAs
         Side population
         Tumorigenesis
         Metastasis
         Chemotherapy resistance
         Pancreatic cancer
         Oncology
         Biomedicine
         general
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      name:Department of General, Visceral und Vascular Surgery, University of Munich, Munich, Germany
      name:Department of General, Visceral und Vascular Surgery, University of Munich, Munich, Germany
      name:Department of General, Visceral und Vascular Surgery, University of Munich, Munich, Germany
      name:Department of General, Visceral und Vascular Surgery, University of Munich, Munich, Germany
      name:Department of General, Visceral und Vascular Surgery, University of Munich, Munich, Germany
      name:Department of General, Visceral und Vascular Surgery, Otto-von-Guericke University, Magdeburg, Germany
      name:Department of General, Visceral und Vascular Surgery, University of Munich, Munich, Germany
      name:Institute of Molecular Immunology, Helmholtz Center Munich, Munich, Germany
      name:Department of General, Visceral und Vascular Surgery, University of Munich, Munich, Germany
      name:Clinical Biochemistry Group, Medizinische Klinik und Poliklinik IV, University of Munich, Munich, Germany
      name:Institute of Molecular Immunology, Helmholtz Center Munich, Munich, Germany
      name:Department of General, Visceral und Vascular Surgery, Otto-von-Guericke University, Magdeburg, Germany
      name:Department of General, Visceral und Vascular Surgery, Otto-von-Guericke University, Magdeburg, Germany
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