Silibinin: An Inhibitor of Mir-181a Gene Expression in Sk-Br-3 Breast Cancer Cell Line
Parvaneh Shahinfar1, Nasrin Motamed2★, Elnaz Birjandian2, Omid Shabanpour3★ Corresponding author
- 1Department of Cell and Molecular Biology, School of Biological Sciences, Kharazmi University, Tehran, IRAN.
- 2School of Biology, College of Science, University of Tehran, Tehran, IRAN.
- 3Faculty of Medicine, Shahrood Islamic Azad University of Medicine, Shahrood, IRAN.
CORRESPONDENCE
Nasrin Motamed
School of Biology, College of Science, University of Tehran, Tehran, IRAN.
Received: 06-01-2017; Revised: 15-02-2017; Accepted: 13-07-2017.
Volume 51, Issue 4 · pp. 597–602 · PUBLISHED 2017 · DOI: 10.5530/ijper.51.4.89
ABSTRACT
Background: Mir-181a has been considered as an attractive molecular target for breast cancer therapy. The main objective of this work is to assess the inhibitory effects of silibinin, a herbal substance, on proliferation, apoptosis and Mir-181a gene expression in human breast cancer cell line SK-BR-3. Materials and Methods: Human breast cancer cell line SK-BR-3 was treated with various concentration of silibinin. Cell viability was assessed by MTT assay and apoptosis by flow cytometry. Expression of human mir-181a gene was measured with real-time PCR. Results: Silibinin inhibits growth of SK-BR-3 cells in a dose- and time-dependent manner and effectively induces apoptosis of SK-BR-3 cells. In addition, silibinin caused a decrease in Mir-181a level. Conclusion: These findings suggest that cell viability along with Mir-181a gene expression in breast cancer cells could be reduced by silibinin. These results suggest that silibinin inhibits the proliferation of SK-BR-3 cells, and it induces apoptosis by down-regulating Mir-181a expression in breast cancer cells.
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Shahinfar, P., Motamed, N., Birjandian, E., & Shabanpour, O. (2017). Silibinin: An Inhibitor of Mir-181a Gene Expression in Sk-Br-3 Breast Cancer Cell Line. Indian Journal of Pharmaceutical Education and Research, 51(4), 597–602. https://doi.org/10.5530/ijper.51.4.89
