Background:
Breast cancer is the most common known malignancy in women and it is therefore very important to prevent and
treat this cancer. In this experimental study, the anti-breast cancer effect of Urginea matrima was investigated.
Method:
Breast cancer cell lines [MCF-7 and MDA-MB231] and L929 normal cells [as a control group] were cultivated in DMEM medium.
Bulb aqueous and hydroalcoholic extracts [70:30] were prepared through maceration method. The cultured cells were treated with different
concentrations [6, 3, 1.5, 0.75, 0.375, 0.187 and 0.093 μg/mL] of U.maritima extracts for 24, 48 and 72 h. Toxicity of the extracts on
cells were examined using MTT test. The Annexin V–FITC Apoptosis Detection Kit was used to evaluate apoptosis and necrosis. Flow cytometry
technique was employed to evaluate the cell cycle and the cell migration was evaluated by Scratch method. Data were analyzed by
GraphPad Prism and SPSS software and P <0.05 was considered significant.
Result:
Results showed that both extracts of U.maritima in the concentration of 1.5 and 3 μg/ ml at 24,48 and 72h presented cytotoxicity
effect on MCF7 cell line . Also, both extracts in the concentration of 3 μg/ ml at 24 and 72h, and in the concentration of 6 μg/ ml at 72h
showed cytotoxicity effect significantly on MDA-MB231 cells. In addition, the plant extracts at the dosage of 3 and 6 μg/ ml induced an accumulation
of G0/G1 cells, as well as reduce in S and G2/M phases in MCF-7 and MDA-MB231 cells. Moreover, the aqueous and hydroalcoholic
of U.maritima extracts at three concentrations [ 1.5, 3 and 6 μg/ ml ] in 24h inhibited the cell migration by 60% up to 70% respectively.
In addition, the content of phenolic compounds in both extracts [aqueous and hydroalcoholic] was 7 mg and 10 mg gallic acid equivalent
per gram of the crude extract, respectively.
Conclusion:
Our results suggest that U.maritima extracts has significant anti-cancer activity against breast cancer cells due to cell cycle arrest
and induction of apoptosis pathway.
MiR-145 inhibits proliferation of primary colon adenocarcinoma cells via induction of apoptosis, cell cycle arrest and inhibition of cell migration
