Document Type : Original Article


1 Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran

2 Department of Biophysics, Institute of Biochemistry and Biophysics, University of Tehran, Tehran, Iran

3 Department of Radiotherapy, Iran University of Medical Sciences (IUMS), Tehran, Iran

4 Department of Photo Healing and Regeneration, Medical Laser Research Center, Yara Institute, ACECR, Tehran, Iran

5 Department of Medical Laser, Medical Laser Research Center, Yara Institute, ACECR, Tehran, Iran


Background: Radiotherapy is a frequently used therapeutic modality for breast cancer. Dalbergin, a natural antioxidant, inhibits carcinogens and tumor progression. In the present study, we investigated the effect of Dalbergin on the response of T47D and MDA-MB-231 breast cancer cell lines to ionizing radiation.
Method: In this experimental in vitro study, doubling time of T47D and MDA-MB-231 were obtained from the growth curve. The cytotoxic effect of Dalbergin on T47D and MDA-MB-231 breast cancer cells were estimated via MTT assay. To determine the clonogenic ability, we treated T47D and MDA-MB-231 with Dalbergin for 48 h prior to irradiation, subsequent to which a colony assay was performed. Real-time polymerase chain reaction was employed to determine the gene expression level.
Results: Dalbergin inhibited proliferation of T47D and MDA-MB-231 in a time- and concentration-dependent manner. Additionally, the most appropriate time for the treatment of these types of cancer cells was found to be 48 h and the drug's concentration in both cell lines was different. The IC50 values of T47D and MDA-MB-231 cells were 0.001 and 0.0001 μM, respectively. Moreover, this drug radiaosensitizes both cell lines effectively compared to the radiation only. Finally, the gene expression level of p53, Bcl-2, and STAT3 were investigated in cancer cells.
Conclusion: Dalbergin showed apoptotic effects probably through the STAT/p53 signaling pathway. Therefore, Dalbergin could be considered as a radiosensitizer and its effects may be owing to increased cell death.


This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination, and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi:10.30476/mejc.2022.91913.1637