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山苏子蛇毒通过 IGF-1 依赖途径、PI3K/AKT 和 ERK 信号诱导人乳腺癌细胞凋亡。

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

机构信息

King Saud University, Riyadh, Saudi Arabia.

出版信息

Cell Immunol. 2012;273(1):10-6. doi: 10.1016/j.cellimm.2011.12.003. Epub 2011 Dec 17.

DOI:10.1016/j.cellimm.2011.12.003
PMID:22218396
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.

摘要

在本研究中,我们评估了来自 Pachycondyla sennaarensis 的 samsum 蚁毒液(SAV)对人乳腺癌细胞系 MCF-7 的抗肿瘤潜力。我们发现 SAV 诱导 MCF-7 细胞生长停滞,而不影响 MCF-10(非致瘤性正常乳腺上皮细胞)和正常 PBMCs 的活力。然后,我们分析了它对 IGF-1 介导的 MCF-7 细胞增殖的影响及其对潜在 IGF-1 信号通路的影响。通过流式细胞术分析,我们显示与未处理的细胞相比,用 SAV 处理的细胞中凋亡细胞的百分比高四倍。更重要的是,SAV 处理诱导肌动蛋白聚合明显减少,随后 IGF-1 介导的细胞增殖明显减少。与未处理的细胞相比,SAV 处理的细胞中 AKT 和 ERK 的磷酸化显著减少,但 p38MAPK 没有减少。我们的数据揭示了 samsum 蚁毒液的独特抗肿瘤作用。

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