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miR-200a Regulates SIRT1 Expression and Epithelial to Mesenchymal Transition (EMT)-like Transformation in Mammary Epithelial Cells

Eades, Gabriel ; Yao, Yuan ; Yang, Muhua ; Zhang, Yongshu ; Chumsri, Saranya ; Zhou, Qun

The Journal of biological chemistry, 2011-07, Vol.286 (29), p.25992-26002 [Periódico revisado por pares]

United States: Elsevier Inc

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Título:
miR-200a Regulates SIRT1 Expression and Epithelial to Mesenchymal Transition (EMT)-like Transformation in Mammary Epithelial Cells
Autor: Eades, Gabriel ; Yao, Yuan ; Yang, Muhua ; Zhang, Yongshu ; Chumsri, Saranya ; Zhou, Qun
Assuntos: Antigens, CD ; Base Sequence ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; Cadherins - genetics ; Cell Line, Tumor ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; DNA Methylation - drug effects ; DNA Methylation - genetics ; Epigenetics ; Epithelial Cell ; Epithelial-Mesenchymal Transition - drug effects ; Epithelial-Mesenchymal Transition - genetics ; Feedback, Physiological - drug effects ; Gene Expression Regulation, Neoplastic - drug effects ; Gene Expression Regulation, Neoplastic - genetics ; Gene Regulation ; Gene Silencing ; HEK293 Cells ; Humans ; Mammary Glands, Human - cytology ; Mammary Glands, Human - drug effects ; Mammary Glands, Human - metabolism ; Mammary Glands, Human - pathology ; MicroRNA ; MicroRNAs - genetics ; Promoter Regions, Genetic - genetics ; SIRT ; Sirtuin 1 - genetics ; Transformation ; Transforming Growth Factor beta - pharmacology
É parte de: The Journal of biological chemistry, 2011-07, Vol.286 (29), p.25992-26002
Descrição: Evidence supports a critical role for microRNAs (miRNAs) in regulation of tissue-specific differentiation and development. Signifying a disruption of these programs, expression profiling has revealed extensive miRNA dysregulation in tumors compared with healthy tissue. The miR-200 family has been established as a key regulator of epithelial phenotype and, as such, is deeply involved in epithelial to mesenchymal transition (EMT) processes in breast cancer. However, the effects of the miR-200 family on transformation of normal mammary epithelial cells have yet to be fully characterized. By examining a TGF-β driven model of transformation of normal mammary epithelium, we demonstrate that the class III histone deacetylase silent information regulator 1 (SIRT1), a proposed oncogene in breast cancer, is overexpressed upon EMT-like transformation and that epigenetic silencing of miR-200a contributes at least in part to the overexpression of SIRT1. We have established the SIRT1 transcript as subject to regulation by miR-200a, through miR-200a targeting of SIRT1 3′-UTR. We also observed SIRT1 and miR-200a participation in a negative feedback regulatory loop. Restoration of miR-200a or the knockdown of SIRT1 prevented transformation of normal mammary epithelial cells evidenced by decreased anchorage-independent growth and decreased cell migration. Finally, we observed SIRT1 overexpression in association with decreased miR-200a in breast cancer patient samples. These observations provide further evidence for a critical tumor suppressive role of the miR-200 family in breast epithelium in addition to identifying a novel regulatory mechanism, which may contribute to SIRT1 up-regulation in breast cancer.
Editor: United States: Elsevier Inc
Idioma: Inglês

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miR-200a Regulates SIRT1 Expression and Epithelial to Mesenchymal Transition (EMT)-like Transformation in Mammary Epithelial Cells

Eades, Gabriel ; Yao, Yuan ; Yang, Muhua ; Zhang, Yongshu ; Chumsri, Saranya ; Zhou, Qun

United States: Elsevier Inc

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