شماره ركورد كنفرانس :
3693
عنوان مقاله :
Induction of apoptosis by silibinin in SKBR3 breast cancer cell line through activation of caspase 3/7
پديدآورندگان :
Maharat Z raha67creator@gmail.com University of Tehran, Collage of Science, School of Biology, Department of Cell and Molecular Biology , Motamed N Motamed2@khayam.ut.ac.ir University of Tehran, Collage of Science, School of Biology, Department of Cell and Molecular Biology , Yazdii E Elmira.yazdii@gmail.com University of kharazmi, Collage of Science, School of Biology, Department of Cell and Molecular Biology
كليدواژه :
Apoptosis , silibinin , breast cancer , SK , BR3 cell
عنوان كنفرانس :
اولين كنگره بين المللي زيست پزشكي ICB2017
چكيده فارسي :
the low 5-year relative survival rate of people with breast cancer is mainly due to its resistance to the conventional treatments. Finding a new drug to treat resistant cancer using any sources, such as herbs, will have huge impact in cancer therapy. Silibinin, the major active component of silymarin extracted from milk thistle, has a strong antioxidant property and weak cytotoxic activity against many types of malignancies. Caspase plays important role in programmed cell death, apoptosis. Since there have been reports that cells undergo apoptosis when exposed to silibinin over time, we investigated cell viability and caspase 3/7 activity in a breast cancer cell line, SKBR3, after treatments by silibinin. Material and methods: In order to investigate the effect of silibinin on breast cancer cell line, SKBR3 cells were treated with different concentrations of drugs (50-350 µM). Cell viability was measured by MTT assay after 24, 48 and 72 hours of treatment and IC50 dosage was calculated (284 µM for 48h). Then, SKBR3 cells treated with selective doses of silibinin (150,250 and 350 µM for 48h) and activation of caspase-3/7 was measured using the Caspase-Glo® 3/7 assay kit. Statistical analysis was performed by GraphPad software. Result: The MTT assay demonstrated that silibinin inhibited SKBR3 cell growth in a time- and dose- dependent manner (P 0.01) and caspase 3/7 activity of SKBR3 cells was enhanced after 48 h exposed to silibinin (P 0.001).Conclusion: These results suggest that silibinin reduces cell viability through apoptotic cell death in SKBR3 cells by activating intrinsic apoptosis pathway. Overall, our data suggest a potential therapeutic value of silibinin to be further developed as an anti-cancer drug.