Protosappanin B promotes apoptosis and causes G1 cell cycle arrest in human bladder cancer cells

被引:23
|
作者
Yang, Xihua [1 ]
Zhao, Lili [1 ]
Zhang, Tingting [2 ]
Xi, Junfeng [1 ]
Liu, Shuze [3 ]
Ren, Liansheng [1 ]
Zheng, Yaqin [1 ]
Zhang, Huanhu [1 ]
机构
[1] Shanxi Med Univ, Affiliated Canc Hosp, Taiyuan 030001, Shanxi, Peoples R China
[2] Shanxi Univ, Res Inst Appl Biol, Taiyuan 030006, Shanxi, Peoples R China
[3] Rensselaer Polytech Inst, Dept Comp Sci, Troy, NY 12180 USA
关键词
CAESALPINIA-SAPPAN; IN-VITRO; LIGNUM; CONSTITUENTS; BRAZILIN; GROWTH; DEATH; HEAD; P53;
D O I
10.1038/s41598-018-37553-z
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The aim of the study was to investigate the effects of protosappanin B on the proliferation and apoptosis of bladder cancer cells. The effects of protosappanin B (12.5, 25, 50, 100, or 200 mu g/mL, 48 h) on proliferation of SV-HUC-1, T24 and 5637 cells was assessed using the MTT assay. The effects of protosappanin B (100, 150, 200, 250, or 300 mu g/mL, 48 h) on cell apoptosis and cell cycle were analyzed using flow cytometry. T24 and 5637 cells treated with 200 mu g/mL protosappanin B showed morphological changes (shrinkage, rounding, membrane abnormalities, and reduced adhesion), but protosappanin B had no proliferation arrest effect on SV-HUC-1 cells. Protosappanin B caused concentration-dependent inhibition of cell growth, with IC50 of 82.78 mu g/mL in T24 cells and 113.79 mu g/mL in 5637 cells. Protosappanin B caused concentration-dependent increases in T24 and 5637 cell apoptosis (100-300 mu g/mL). The effects of protosappanin B on the cell cycle in both cell types was G(1) arrest with reductions in the proportion of S-phase cells and proliferation index. A proteomics analysis showed that protosappanin B modulated a number of genes involved in the cell cycle. In conclusion, protosappanin B inhibits the proliferation and promotes the apoptosis of T24 and 5637 human bladder cancer cells in a concentration-dependent manner, possibly via interference with cell cycle regulation, preventing G(1)-to-S transition.
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页数:10
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