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Genistein-induced mir-23b expression inhibits the growth of breast cancer cells

AIM OF THE STUDY: Genistein, an isoflavonoid, plays roles in the inhibition of protein tyrosine kinase phosphorylation, induction of apoptosis, and cell differentiation in breast cancer. This study aims to induce cellular stress by exposing genistein to determine alterations of miRNA expression prof...

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Detalles Bibliográficos
Autores principales: Avci, Cigir Biray, Susluer, Sunde Yilmaz, Caglar, Hasan Onur, Balci, Tugce, Aygunes, Duygu, Dodurga, Yavuz, Gunduz, Cumhur
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4507883/
https://www.ncbi.nlm.nih.gov/pubmed/26199568
http://dx.doi.org/10.5114/wo.2014.44121
Descripción
Sumario:AIM OF THE STUDY: Genistein, an isoflavonoid, plays roles in the inhibition of protein tyrosine kinase phosphorylation, induction of apoptosis, and cell differentiation in breast cancer. This study aims to induce cellular stress by exposing genistein to determine alterations of miRNA expression profiles in MCF-7 cells. MATERIAL AND METHODS: XTT assay and trypan blue dye exclusion assays were performed to examine the cytotoxic effects of genistein treatment. Expressions of miRNAs were quantified using Real-Time Online RT-PCR. RESULTS: The IC(50) dose of genistein was 175 μM in MCF-7 cell, line and the cytotoxic effect of genistein was detected after 48 hours. miR-23b was found to be up-regulated 56.69 fold following the treatment of genistein. It was found that miR-23b was upregulated for MCF-7 breast cancer cells after genistein treatment. CONCLUSIONS: Up-regulated ex-expression of miR-23b might be a putative biomarker for use in the therapy of breast cancer patients. miR-23b up-regulation might be important in terms of response to genistein.