Doxorubicin Induces Apoptosis through down Regulation of miR-21 Expression and Increases miR-21 Target Gene Expression in MCF-7 Breast Cancer Cells

Tofigh, Roghayeh and Akhavan, Saeedeh and Tarban, Nastaran and Sadrabadi, Amin Ebrahimi and Jalili, Arsalan and Moridi, Kaykhosro and Tutunchi, Sara (2017) Doxorubicin Induces Apoptosis through down Regulation of miR-21 Expression and Increases miR-21 Target Gene Expression in MCF-7 Breast Cancer Cells. International Journal of Clinical Medicine, 08 (06). pp. 386-394. ISSN 2158-284X

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Abstract

miRNAs play an important regulatory role in variety of cellular functions and several diseases, including cancer. MicroRNA-21 (miR-21) is overexpressed in almost all types of human cancers. Studies revealed that the knockdown of miR-21 results in reduced tumor cell growth, cell cycle arrest and cell apoptosis. In this study, we evaluated the effect of doxorubicin on miR-21 expression in mcf-7 breast cancer cells. miRNA was extracted from mcf-7 cells treated with doxorubicin and untreated cells using miRNeasy Kit (Qiagen) according to the manufacturer’s instructions. cDNA synthesis was performed using miScript II RT Kit (Qiagen) and Real Time-PCR was performed using Real Q Plus 2x Master Mix Green-(Ampliqon, Denmark). The relative expression of miR-16 and miR-21 was calculated using comparative Ct method. All tests were run in triplicate to minimize the experimental errors. Samples with a Ct > 37 were excluded from the analysis. Statistically, a significant decrease in cell proliferation of mcf-7 cells was found in doxorubicin group compared with control groups 24 hours after transfection, dose dependently (p value< 0.001). After 24 hours, Doxorubicin (100 μm) significantly decreased miR-21 expression in mcf-7 cells (p = 0.0001). Also, the expression of caspase 9 significantly increased after Doxorubicin (100 μm) treatment (p = 0.0003). Together, these findings indicate that miR-21 plays a key role in regulating cell apoptosis in mcf-7 cells and may serve as a target for effective therapies.

Item Type: Article
Subjects: Eurolib Press > Medical Science
Depositing User: Managing Editor
Date Deposited: 21 Jan 2023 05:15
Last Modified: 26 Feb 2024 04:13
URI: http://info.submit4journal.com/id/eprint/1101

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