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细胞因子对前列腺癌细胞活力和死亡的影响。

Cytokine effects on cell viability and death of prostate carcinoma cells.

作者信息

Chondrogiannis Georgios, Kastamoulas Michalis, Kanavaros Panagiotis, Vartholomatos Georgios, Bai Maria, Baltogiannis Dimitrios, Sofikitis Nikolaos, Arvanitis Dimitrios, Galani Vasiliki

机构信息

Department of Anatomy-Histology-Embryology, Medical School, University of Ioannina, 45110 Ioannina, Greece.

Laboratory of Hematology, University Hospital of Ioannina, 45500 Ioannina, Greece.

出版信息

Biomed Res Int. 2014;2014:536049. doi: 10.1155/2014/536049. Epub 2014 May 29.

DOI:10.1155/2014/536049
PMID:24982891
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4058150/
Abstract

We analyzed the effects of IL-13, IFN- γ , and IL-1 β on cell viability and death of LNCaP and PC-3 cells and major signaling pathways involved in these effects. Significant increase of LNCaP cell death (apoptotic and necrotic) and increased levels of active caspase 3 were observed in cells treated with inhibitors of ERK 1/2 (UO126) and p38 (SB203580) prior to IL-1 β treatment in comparison to cells treated with UO126, SB203580, or IL-1 β alone. Significant increase of LNCaP but not PC-3 cell death was detected after treatment with LY-294002 (inhibitor of phosphatidylinositol 3-kinase). No significant increase of LNCaP and PC-3 cell death was observed after treatment with SP600125 (inhibitor of JNK), SB203580 (inhibitor of p38), UO126 (inhibitor of ERK 1/2), or BAY 11-7082 (inhibitor of NF- κ B). Reduced c-FLIPL expression was observed in LNCaP cells treated with LY-294002. The significant potentiation of LNCaP cell death by inhibition of ERK 1/2, p38, and PI3-K pathways may provide a rationale for therapeutic approach in androgen-dependent prostate cancer.

摘要

我们分析了白细胞介素-13（IL-13）、干扰素-γ（IFN-γ）和白细胞介素-1β（IL-1β）对LNCaP和PC-3细胞活力及死亡的影响，以及参与这些效应的主要信号通路。与单独用UO126、SB203580或IL-1β处理的细胞相比，在IL-1β处理前用细胞外信号调节激酶1/2（ERK 1/2）抑制剂（UO126）和p38抑制剂（SB203580）处理的细胞中，观察到LNCaP细胞死亡（凋亡和坏死）显著增加，且活性半胱天冬酶3水平升高。用磷脂酰肌醇3-激酶抑制剂LY-294002处理后，检测到LNCaP细胞死亡显著增加，但PC-3细胞死亡未增加。用应激活化蛋白激酶（JNK）抑制剂SP600125、p38抑制剂SB203580、ERK 1/2抑制剂UO126或核因子κB（NF-κB）抑制剂BAY 11-7082处理后，未观察到LNCaP和PC-3细胞死亡显著增加。在用LY-294002处理的LNCaP细胞中观察到c-FLIPL表达降低。抑制ERK 1/2、p38和磷脂酰肌醇3-激酶（PI3-K）通路对LNCaP细胞死亡的显著增强作用可能为雄激素依赖性前列腺癌的治疗方法提供理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546a/4058150/601ac927f526/BMRI2014-536049.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546a/4058150/e45cd2c78557/BMRI2014-536049.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546a/4058150/c9db7dea73dc/BMRI2014-536049.002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546a/4058150/2efca01d9924/BMRI2014-536049.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546a/4058150/ce42b67c666d/BMRI2014-536049.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546a/4058150/57f3d93e77d1/BMRI2014-536049.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546a/4058150/b8ae6c06bb33/BMRI2014-536049.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546a/4058150/de16c19b786f/BMRI2014-536049.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546a/4058150/601ac927f526/BMRI2014-536049.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546a/4058150/e45cd2c78557/BMRI2014-536049.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546a/4058150/c9db7dea73dc/BMRI2014-536049.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546a/4058150/52a61c0892d0/BMRI2014-536049.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546a/4058150/2efca01d9924/BMRI2014-536049.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546a/4058150/ce42b67c666d/BMRI2014-536049.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546a/4058150/57f3d93e77d1/BMRI2014-536049.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546a/4058150/b8ae6c06bb33/BMRI2014-536049.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546a/4058150/de16c19b786f/BMRI2014-536049.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546a/4058150/601ac927f526/BMRI2014-536049.009.jpg

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