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      miR-21-mediated tumor growth.

      Oncogene

      Animals, Apoptosis, Breast, metabolism, Breast Neoplasms, genetics, pathology, Cell Proliferation, Female, Gene Expression Regulation, Neoplastic, Humans, Mice, Mice, Nude, MicroRNAs, antagonists & inhibitors, physiology, Oligonucleotides, Antisense, pharmacology, Proto-Oncogene Proteins c-bcl-2, RNA Processing, Post-Transcriptional, RNA, Messenger, Xenograft Model Antitumor Assays

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          Abstract

          MicroRNAs (miRNAs) are approximately 22 nucleotide non-coding RNA molecules that regulate gene expression post-transcriptionally. Although aberrant expression of miRNAs in various human cancers suggests a role for miRNAs in tumorigenesis, it remains largely unclear as to whether knockdown of a specific miRNA affects tumor growth. In this study, we profiled miRNA expression in matched normal breast tissue and breast tumor tissues by TaqMan real-time polymerase chain reaction miRNA array methods. Consistent with previous findings, we found that miR-21 was highly overexpressed in breast tumors compared to the matched normal breast tissues among 157 human miRNAs analysed. To better evaluate the role of miR-21 in tumorigenesis, we transfected breast cancer MCF-7 cells with anti-miR-21 oligonucleotides and found that anti-miR-21 suppressed both cell growth in vitro and tumor growth in the xenograft mouse model. Furthermore, this anti-miR-21-mediated cell growth inhibition was associated with increased apoptosis and decreased cell proliferation, which could be in part owing to downregulation of the antiapoptotic Bcl-2 in anti-miR-21-treated tumor cells. Together, these results suggest that miR-21 functions as an oncogene and modulates tumorigenesis through regulation of genes such as bcl-2 and thus, it may serve as a novel therapeutic target.

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          Journal
          17072344
          10.1038/sj.onc.1210083

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