Document Type : Research articles
Authors
1 Department of Biology, Sciences 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, Tehran, Iran
Abstract
Background: Breast cancer is an important cause of death among women. Prevention of cancer through dietary intervention has recently received increasing interest. Lately, dietary polyphenols have gained much attention for their health benefits, including anticancer properties. Dalbergin as a polyphenol is synthesized from a common neoflavene intermediate.
Objectives: This study aimed to examine whether dalbergin can be useful in the chemotherapy of estrogen receptor-positive T47D cell line.
Methods: This experimental study was performed at the Laboratory of Biophysics and Molecular Biology, the Institute of Biochem- istry and Biophysics, University of Tehran, Tehran, Iran, from October 2017 to November 2019. The doubling time of T47D cells was obtained from the growth curve. The cytotoxic effect of dalbergin on T47D breast cancer cells was evaluated. To assess the clonogenic ability, T47D cells were treated with dalbergin for 48 hours and then, the colony assay was performed. A Real-Time PCR was used to determine the transcription levels of p53, Bcl-2, and STAT3 genes.
Results: The doubling time of T47D cells was 28.02 ± 4.22 hours (P < 0.05). Dalbergin decreased the viability of the T47D cell line. The half-maximal inhibitory concentration (IC50) values of dalbergin for T47D cells were found to be 1 μM in 24 hours, 0.001 μM in 48 hours, and 0.00001 μM in 72 hours of treatment (P < 0.05). In the clonogenic assay, 0.001 μM dalbergin for 48 hours could reduce the surviving fraction of T47D cells (P < 0.05). Additionally, dalbergin could change the mRNA levels of p53, Bcl-2, and STAT3 genes (P < 0.05).
Conclusions: Our results indicated that dalbergin has some anticancer effects probably through inducing apoptosis in cancerous cells by changing mRNA levels of apoptosis-related proteins.
Keywords
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