Malvidin induced anticancer activity in human colorectal HCT-116 cancer cells involves apoptosis, G2/M cell cycle arrest and upregulation of p21WAFI

被引:0
|
作者
Xu, Hongtuan [1 ]
Zhang, Jian [1 ]
Huang, Huaxing [3 ]
Liu, Linxiang [4 ]
Sun, Yunliang [2 ]
机构
[1] Ganyu Peoples Hosp Lianyungang, Dept Gen Surg, Liangyungang 222100, Jiangsu, Peoples R China
[2] Ganyu Peoples Hosp Lianyungang, Dept Gastroenterol, Liangyungang 222100, Jiangsu, Peoples R China
[3] Nanjing Med Univ, Affiliated Hosp 1, Dept Gen Surg, Nanjing 210029, Jiangsu, Peoples R China
[4] Nanjing Med Univ, Affiliated Hosp 1, Dept Oncol, Nanjing 210029, Jiangsu, Peoples R China
关键词
Colorectal cancer; cell cycle arrest; apoptosis; malvidin; CARCINOMA-CELLS; DNA-DAMAGE; EXPRESSION; PATHWAY; ACID; LINE;
D O I
暂无
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Colorectal carcinoma is one of the most frequently detected cancers around the globe with an incidence of 1.4 million. Despite advances in the therapeutics and surgical interventions, there is a pressing need to explore safer and more effective therapeutic modalities. In the recent past natural products have gained attention for their diverse bioactivities. In the present study we evaluated the anticancer activity of malvidin, a natural product of plant origin, against human colorectal HCT-116 cancer and FR-2 normal human cell lines. The results of the present study revealed that malvidin exhibited an IC50 of 15 mu M against colorectal cancer HCT-116 cell line as compared to the IC50 of 65 mu M against the normal human FR-2 cell line. Malvidin caused significant inhibition of colony formation and triggered apoptosis in HTC-116 cells. Additionally, malvidin treatment induced G2/M cell cycle arrest which was also associated with concentration-dependent inhibition of cell cycle related proteins and upregulation of p21WAFI. Takentogether, we propose that malvidin exhibited significant anticancer activity against colorectal cancer cells and may prove as an important lead molecule in cancer chemotherapy.
引用
收藏
页码:1734 / 1741
页数:8
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