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Volume 13, Issue 2 (Iranian Journal of Breast Disease 2020)                   ijbd 2020, 13(2): 37-48 | Back to browse issues page


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Bahman Jahromi E, Jafaarnejad L, Vahdani M, Zolghadri S. Toxicity Effect of Bromoacetic Acid on MCF7 Breast Cancer Cell Line and Analysis of Expression of Apoptosis-Associated Genes. ijbd 2020; 13 (2) :37-48
URL: http://ijbd.ir/article-1-770-en.html
1- Department of Biology, Jahrom Branch, Islamic Azad University, Jahrom, Iran
2- Msc Student, Department of Biology, Jahrom Branch, Islamic Azad University, Jahrom, Iran
3- Department of Biology, Jahrom Branch, Islamic Azad University, Jahrom, Iran , szjahromi@yahoo.com
Abstract:   (2946 Views)
Introduction: Cancer, the uncontrolled division of cells, occurs because of environmental factors and genetic disorders. Breast cancer is the most common cancer and the second leading cause of cancer death in women. Four categories of key genes, including oncogenes, tumor suppressor genes, repairing genes, and programmed– cell death genes, contribute to cancer development. Bromoacetic acid is a chemical compound that is produced both artificially and by bacterial fermentation.
Methods: To investigate the effectiveness of bromoacetic acid in inhibiting the MCF7 cell line proliferation, the MTT assay was done and the expression of genes responsible for the regulation of apoptosis, including BAK, CASP3, CASP8, and BIM, was measured after 24, 48, and 72 hours of cell treatment with 2.5 µg/ml of bromoacetic acid using real–time PCR.
Results: The results of the gene expression assays showed that bromoacetic acid treatment increased the expression of key genes BAK, CASP3, and, CASP8. However, the expression of BIM decreased at all three time points compared with controls.
Conclusion: bromoacetic acid can induce cell death via intrinsic and extrinsic apoptosis pathways.
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Conclusion: bromoacetic acid can induce cell death via intrinsic and extrinsic apoptosis pathways.
Type of Study: Research |
Received: 2019/08/14 | Accepted: 2020/03/1 | Published: 2020/08/19

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