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We began analyzing https://www.tandfonline.com/doi/abs/10.4161/rna.6.5.10079, but it redirected us to https://www.tandfonline.com/doi/abs/10.4161/rna.6.5.10079. The analysis below is for the second page.

Title[redir]:
MicroRNA-125a represses cell growth by targeting HuR in breast cancer: RNA Biology: Vol 6, No 5
Description:
MicroRNAs (miRNAs) are a class of naturally occurring, small, non-coding RNAs that control gene expression during development, normal cell function, and disease. Although there is emerging evidence...

Matching Content Categories {πŸ“š}

  • Education
  • Science
  • Health & Fitness

Content Management System {πŸ“}

What CMS is doi.org built with?

Custom-built

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Traffic Estimate {πŸ“ˆ}

What is the average monthly size of doi.org audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


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Keywords {πŸ”}

source, cancer, cell, expression, hur, microrna, research, breast, human, journal, protein, mira, carcinoma, cells, mrna, clinical, rna, tumor, factor, growth, gene, migration, taylor, francis, group, page, mirnas, prognostic, target, carcinogenesis, cyclooxygenase, genes, sciences, oncogene, targets, invasion, journals, biology, targeting, open, micrornas, function, binding, increased, proliferation, overexpression, suppressor, molecular, downregulation, proceedings,

Topics {βœ’οΈ}

u-rich-element-dependent manner source predicted microrna-binding sites rna-binding protein hur precursor microrna‐155/bic rna micro-rna mir-125a embryonic-lethal abnormal vision establishing mir-125a expression mrna stability source microrna targets source twitter page taylor cancer research polymorphisms human breast cancer mrna binding proteins open cancer research microrna-21 clinical cancer research francis group biological chemistry mirnas inhibited cell growth human prostate carcinoma aib1 mrna source cancer research expression cancer research overexpression breast cancer risk clinical behavior source control gene expression tumor suppressor higher tumor grade advanced clinical stage mir-125b source cyclin e1 deregulation colon carcinogenesis source human disease source cancer cell survival mir-125a overexpression microrna expression signature gene reporter assays merkel cell carcinoma Ξ²-actin mrna rna hur contributes patient survival source limited understanding cox-2 expression source increased cyclooxygenase-2 expression receive personalised research gastric cancer burkitt lymphoma source premenopausal women source normal skin source prometheus gift source

Schema {πŸ—ΊοΈ}

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            name:Volume 6, Issue 5
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            name:MicroRNA-125a represses cell growth by t ....
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PublicationIssue:
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      issueNumber:5
      datePublished:2009-11-01
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            1547-6286
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      articleSection:Research Paper
      name:MicroRNA-125a represses cell growth by targeting HuR in breast cancer
      headline:MicroRNA-125a represses cell growth by targeting HuR in breast cancer
      abstract:MicroRNAs (miRNAs) are a class of naturally occurring, small, non-coding RNAs that control gene expression during development, normal cell function, and disease. Although there is emerging evidence that some miRNAs can function as oncogenes or tumor suppressors, there is limited understanding of the role of miRNAs in cancer. In this study, we observed that the expression of miR-125a was inversely correlated with HuR expression in several different breast carcinoma cell lines. HuR is a stress-induced RNA binding protein whose expression is elevated or localization perturbed in several different cancers. Increased cytoplasmic localization of HuR is a prognostic marker in breast cancer. Real time PCR and gene reporter assays indicated that HuR was translationally repressed by miR-125a. Re-establishing miR-125a expression in breast cancer cells decreased HuR protein level and inhibited cell growth. Using MCF-7 breast cancer cells, we further clarified that miR-125a inhibited cell growth via a dramatic suppression of cell proliferation and promotion of apoptosis. In addition, cell migration was also inhibited by miR-125a overexpression. Importantly, the repression of cell proliferation and migration engendered by miR-125a was partly rescued by HuR re-expression. Our results suggest that miR-125a may function as a tumor suppressor for breast cancer, with HuR as a direct and functional target.
      description:MicroRNAs (miRNAs) are a class of naturally occurring, small, non-coding RNAs that control gene expression during development, normal cell function, and disease. Although there is emerging evidence that some miRNAs can function as oncogenes or tumor suppressors, there is limited understanding of the role of miRNAs in cancer. In this study, we observed that the expression of miR-125a was inversely correlated with HuR expression in several different breast carcinoma cell lines. HuR is a stress-induced RNA binding protein whose expression is elevated or localization perturbed in several different cancers. Increased cytoplasmic localization of HuR is a prognostic marker in breast cancer. Real time PCR and gene reporter assays indicated that HuR was translationally repressed by miR-125a. Re-establishing miR-125a expression in breast cancer cells decreased HuR protein level and inhibited cell growth. Using MCF-7 breast cancer cells, we further clarified that miR-125a inhibited cell growth via a dramatic suppression of cell proliferation and promotion of apoptosis. In addition, cell migration was also inhibited by miR-125a overexpression. Importantly, the repression of cell proliferation and migration engendered by miR-125a was partly rescued by HuR re-expression. Our results suggest that miR-125a may function as a tumor suppressor for breast cancer, with HuR as a direct and functional target.
      author:
            type:Person
            name:Xun Guo
            type:Person
            name:Rebecca Hartley
            type:Person
            name:Yuehan Wu
            type:Person
            name:Rebecca Hartley
      pageStart:575
      pageEnd:583
      datePublished:2009-11-01
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         type:Organization
         name:Taylor & Francis
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      name:Rebecca Hartley
      name:Yuehan Wu
      name:Rebecca Hartley
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      name:Taylor & Francis
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