Genistein-induced Mir-23b Expression Inhibits the Growth of Breast Cancer Cells

Overview

Journal Contemp Oncol (Pozn)

Publisher Termedia

Specialty Oncology

Date 2015 Jul 23

PMID 26199568

Citations 17

Authors

Cigir Biray Avci

Sunde Yilmaz Susluer

Hasan Onur Caglar

Tugce Balci

Duygu Aygunes

Yavuz Dodurga

Cumhur Gunduz

Affiliations

Soon will be listed here.

Abstract

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 IC50 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.

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