Abstract |
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 pro-apoptotic effects, significant reductions were also observed in the phosphorylation of AKT 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.
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Authors | Gamal Badr, Olivier Garraud, Maha Daghestani, Mohammed Saleh Al-Khalifa, Yolande Richard |
Journal | Cellular immunology
(Cell Immunol)
Vol. 273
Issue 1
Pg. 10-6
( 2012)
ISSN: 1090-2163 [Electronic] Netherlands |
PMID | 22218396
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2011 Elsevier Inc. All rights reserved. |
Chemical References |
- Ant Venoms
- Insulin-Like Growth Factor I
- Phosphatidylinositol 3-Kinase
- Proto-Oncogene Proteins c-akt
- Extracellular Signal-Regulated MAP Kinases
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Topics |
- Ant Venoms
(pharmacology)
- Apoptosis
(drug effects)
- Breast Neoplasms
(drug therapy, enzymology, pathology)
- Cell Growth Processes
(drug effects)
- Cell Line, Tumor
- Cell Survival
(drug effects)
- Extracellular Signal-Regulated MAP Kinases
(metabolism)
- Female
- Flow Cytometry
- Humans
- Immunoblotting
- Insulin-Like Growth Factor I
(metabolism)
- MAP Kinase Signaling System
- Phosphatidylinositol 3-Kinase
(metabolism)
- Phosphorylation
- Proto-Oncogene Proteins c-akt
(metabolism)
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