Effect of Emodin on Expression of VEGF-A and VEGFR_2 Genes in Human Breast Carcinoma MCF-7 Cell

Tumor angiogenesis is an important procedure for the tumor development as it confirms oxygen and nutrients source to increase cells through the expansion of new blood vessels, potentially causing cancer development and metastasis. Emodin, a tyrosine kinase inhibitor, is an innate anthraquinone derivative found in the roots and rhizomes of several plants. Pharmacological studies have revealed that emodin displays various biological roles, such as anti-inflammatory, antibacterial and anticancer action. Studies have confirmed that emodin prevents cell growth in some types of cancer cells. Therefore, inhibition of angiogenesis is a new strategy for cancer treatment.
In this study, we aimed to determine the effect of emodin on expression of VEGF-A and VEGFR-2 genes in MCF-7 cell line.
Comparative cell viability was measured by MTT assay after treatment with different concentrations of emodin (0, 10, 20, 30, 40 and 50μM) for 24, 48, 72 hours. To investigate apoptosis in cells treated with emodin (0, 10, 20, 30, 40 and 50 µM), flow cytometry was used. Finally, alterations in expression of VEGF-A and VEGFR-2genes were analyzed by real time PCR.
Emodin showed an anti-cancer effect with concentration of 20 μM as IC50 in MCF-7 cells. Emodin induced apoptosis and significantly reduced mRNA level of VEGF-A and VEGFR-2 gene in MCF-7 cell line in a dose dependent manner.
Based on results obtained, emodin significantly reduced mRNA level of VEGF-A and VEGFR-2 gene in MCF-7 cell line in a dose dependent manner.