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The emerging role of miR-200 family of MicroRNAs in epithelial-mesenchymal transition and cancer metastasis

Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA.
RNA biology (Impact Factor: 5.38). 08/2008; 5(3):115-9. DOI: 10.4161/rna.5.3.6558
Source: PubMed

ABSTRACT MicroRNAs (miRNAs) play essential roles in many physiological and pathological processes, including tumor development, by regulating the expression of a plethora of mRNAs. Although the importance of miRNAs in tumorigenesis is well established, only recently have reports elucidated miRNAs as promoters or suppressors of metastasis. The miR-200 family has been shown to inhibit the initiating step of metastasis, epithelial-mesenchymal transition (EMT), by maintaining the epithelial phenotype through direct targeting of transcriptional repressors of E-cadherin, ZEB1 and ZEB2. These findings shed light into a miRNA-mediated regulatory pathway that influences EMT in a developmentally and pathologically relevant setting.

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    • "In our result, mir-200a, mir-200b and mir-429 were all up-regulated, which indicates the important role of the miR-200 family in podocyte differentiation. In fact, series researchers have reported the pivotal role of miR-200 family in development and disease (Choi et al. 2008; Korpal and Kang 2008). To our surprise, mir-200a, mir-200b and mir-429 were all involved in the regulated microRNAs that were potentially regulated by the three transcription factors P53, SP1 and CREB (Table 1). "
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    Molecular Genetics and Genomics 11/2014; 290(3). DOI:10.1007/s00438-014-0960-z · 2.83 Impact Factor
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    • "Patients with tumours that express these receptors often have a better prognosis because they respond well to treatments such as Tamoxifen. We hypothesize that methylation at P2, is likely to be associated with a lower level of miRNA expression, resulting in a more aggressive tumour (Korpal and Kang, 2008) that is unresponsive to these therapies and generally associated with poor prognosis. Using publicly available ER Chip-sequence data (Schmidt et al., 2010), ER bound to a putative ER response element just downstream of P1 upon ER stimulation in MCF7s (Figure 6e). "
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    Oncogene 01/2012; 31(38):4182-95. DOI:10.1038/onc.2011.584 · 8.56 Impact Factor
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    • "In addition, a recent report showed that gemcitabine sensitivity can be induced in pancreatic cancer cells through modulation of miR-200 and miR-21 expression by curcumin (Ali et al. 2010). The miR-200 family has been shown to inhibit the EMT, the initiating step of metastasis, by maintaining the epithelial phenotype through direct targeting of the transcriptional repressors of E-cadherin, ZEB1, and ZEB2 (Korpal and Kang 2008). Therefore, targeting specific miRNAs could be a novel therapeutic approach for the treatment of cancers, especially by eliminating cancer stem cells or EMT-type cells that are typically drug resistant. "
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