Author/Authors :
Omrani Mir Davood نويسنده , Ahmadi Farzaneh نويسنده Department of Horticulture, Rafsanjan Branch, Islamic Azad University, Rafsanjan, Iran , Kazerouni Faranak نويسنده Department of Laboratory Medicine, Faculty of Paramedical Sciences, Shahid Beheshti University, MC, Tehran , Dehghan Nayeri Nasrin نويسنده Department of Proteomics, Faculty of Paramedical Sciences, Shahid Beheshti University of Medical Sciences, Tehran , Rahimipour Ali نويسنده Proteomics Research Center, Faculty of Paramedical Sciences , Shanaki Mehrnoosh نويسنده Department of Laboratory Medicine, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran Shanaki Mehrnoosh , Rezapour Kalkhoran Maryam نويسنده Department of Medical Laboratory Sciences, School of
Allied Medical Sciences, Shahid Beheshti University of Medical
Sciences, Tehran, IR Iran , Younesian Ommolbanin نويسنده Department of Medical Laboratory Sciences, School of
Allied Medical Sciences, Shahid Beheshti University of Medical
Sciences, Tehran, IR Iran , Cheshmi Fatemeh نويسنده Department of Medical Laboratory Sciences, School of
Allied Medical Sciences, Shahid Beheshti University of Medical
Sciences, Tehran, IR Iran
Abstract :
Background The poor prognosis of breast cancer is due to its
resistance to the conventional treatments. Therefore, researchers are
studying about herbs which have anticancer effects. Emodin is a
hydroxy-anthraquinone that is found in many medicinal plants and has
biological and anticancer effects. According to previous studies, it
inhibited the growth of cancer cells by apoptosis. Objectives In this
study, we aimed to determine the effect(s) of emodin on growth and
proliferation of SKBR3 cancer cells. Methods SKBR3 cells were cultivated
for 24 hours. Then different concentrations of emodin (0, 10, 25 and 50
µM) were added to the test wells and incubated for 24, 48 and 72 hours.
Cell viability was examined by MTT assay after 24, 48 and 72 hours.
Apoptosis was determined in cells treated with emodin (0, 10, 25 and 50
µM) using flow cytometric assay. Alterations in expression of
apoptotic-related genes (Caspase 3, 8, 9, Bcl2 and Bax) were determined
by real time PCR. Caspase 3 activity was measured using a colorimetric
assay. Results Emodin had inhibitory effects on the proliferation of
SKBR3 cells with IC50 value of 25 µM. Emodin
induced apoptosis and increased the mRNA expression of Caspase 3, 8, 9
and Bax and decreased the mRNA expression of Bcl2 in SKBR3 cells. It
also increased the activity of Caspase 3. Conclusions Emodin had an
inhibitory effect on the growth of SKBR3 cell line in a dose and time
dependent manner. This study indicated that emodin induces apoptosis in
SKBR3 cells through the alterations of the expression of
apoptosis-related genes and increases the activity of Caspase 3.
