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MiR-221/-222 differentiate prognostic groups in advanced breast cancers and influence cell invasion.

Br. J. Cancer 109, 2714-2723 (2013)
Verlagsversion Volltext DOI PMC
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Background:MiR-221/-222 are frequently overexpressed in breast cancer and are associated with increased malignancy. The specific modification of microRNAs (miRNAs) expression could be a promising strategy in breast cancer therapy, leading to the suppression of tumourigenic processes in tumour cells.Methods:MiR-221/-222 expressions were analysed in 86 breast cancer tissues by quantitative RT-PCR and tested for correlation with immunohistochemistry data and clinical follow-up. In vitro assays were conducted using human breast cancer cell lines with lentiviral overexpression of miR-221/-222.Results:In tumour tissues, miR-221/-222 were associated with the occurrence of distant metastases. In particular, high levels of miR-221 were revealed to have a high prognostic impact for the identification of significantly different groups with advanced tumours. MiR-221/-222 overexpression strongly increased cell proliferation and invasion in vitro. Following miR-221/-222 overexpression an increased uPAR expression and cell invasion were observed.Conclusion:This study demonstrates a significant role for highly expressed miR-221/-222 in advanced breast cancers allowing for the identification of significantly different prognostic groups, particularly for HER2-positive and lymph-node-positive breast cancers. Considering that miR-221/-222 are strongly involved in cell invasion, these miRNAs may be promising markers for breast cancer prognosis and therapy.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Therapy ; Prognosticator ; Prognosis ; Metastasis ; Malignancy ; Mir-221 ; Mir-222 ; Urokinase-type Plasminogen Activator System ; Upar; Urokinase Plasminogen-activator ; Estrogen-receptor-alpha ; Messenger-rna ; Tamoxifen Resistance ; Down-regulation ; Expression ; Micrornas ; Metastasis ; Survival ; Mir-222
ISSN (print) / ISBN 0007-0920
e-ISSN 1532-1827
Zeitschrift British Journal of Cancer BJC
Quellenangaben Band: 109, Heft: 10, Seiten: 2714-2723 Artikelnummer: , Supplement: ,
Verlag Nature Publishing Group
Begutachtungsstatus