Human breast carcinoma cells are induced to apoptosis by samsum ant venom through an IGF-1-dependant pathway, PI3K/AKT and ERK signaling

被引:38
作者
Badr, Gamal [1 ,3 ]
Garraud, Olivier [1 ,4 ]
Daghestani, Maha [2 ]
Al-Khalifa, Mohammed Saleh [2 ]
Richard, Yolande [5 ]
机构
[1] King Saud Univ, Grad Studies & Res Visiting Prof Program, Riyadh 11451, Saudi Arabia
[2] King Saud Univ, Dept Zool, Coll Sci, Riyadh 11451, Saudi Arabia
[3] Assiut Univ, Dept Zool, Fac Sci, Assiut, Egypt
[4] Univ Lyon, EA3064 GIMAP, F-42023 St Etienne 2, France
[5] CNRS, INSERM, Dept Immunol, Inst Cochin,UMR 8104,U1016, F-75014 Paris, France
关键词
Ant; Apoptosis; Breast cancer; Cell signaling; Venom; CANCER CELLS; MCF-7; CELLS; GROWTH; PROGRESSION; ANAPHYLAXIS; MOTILITY; KINASE; MODEL;
D O I
10.1016/j.cellimm.2011.12.003
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
In the present study we evaluated the anti-tumor potential of samsum ant venom (SAV) from Pachycondyla sennaarensis on the human breast carcinoma cell line MCF-7. We found that SAV induced growth arrest of MCF-7 cells without affecting the viability of MCF-10 (non-tumorigenic normal breast epithelial cells) and normal PBMCs. We then analyzed its impact on IGF-1-mediated MCF-7 cell proliferation and its effect on the underlying IGF-1 signaling pathways. Using flow cytometry analysis, we showed that the percentage of apoptotic cells was fourfold higher in SAV-treated cells as compared to untreated cells. More importantly, treatment with SAV induced a marked reduction in actin polymerization and a subsequent marked reduction in IGF-1-mediated cell proliferation. In addition to growth-inhibitory and proapoptotic effects, significant reductions were also observed in the phosphorylation of Ala and ERK, but not p38MAPK, in SAV-treated cells as compared to untreated cells. Our data reveal unique anti-tumor effects of samsum ant venom. (C) 2011 Elsevier Inc. All rights reserved.
引用
收藏
页码:10 / 16
页数:7
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