The Proinflammatory Cytokine, IL-6, and its Interference with bFGF Signaling and PSMA in Prostate Cancer Cells

被引:12
|
作者
Ben Jemaa, Awatef [1 ]
Sallami, Sataa [2 ]
Ramarli, Dunia [3 ]
Colombatti, Marco [3 ]
Oueslati, Ridha [1 ]
机构
[1] Univ Carthage, Unit Immunol & Microbiol Environm & Carcinogenesi, Fac Sci Bizerte, Bizerte 7021, Zarzouna, Tunisia
[2] Hosp La Rabta Tunis, Dept Urol, Tunis, Tunisia
[3] Giovanni Battista Rossi Hosp, Verona, Italy
关键词
proinflammatory cytokine; IL-6; bFGF; PSMA; MAPKs; AKT; angiogenesis; prostate cancer; FIBROBLAST-GROWTH-FACTOR; MEMBRANE ANTIGEN; ENDOTHELIAL-CELLS; PROTEIN-KINASE; INTERLEUKIN-6; EXPRESSION; PROLIFERATION; ANGIOGENESIS; MIGRATION; LINE;
D O I
10.1007/s10753-012-9586-7
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The aim of the present work was to study the expression of the proinflammatory cytokine, interleukin-6 (IL-6), mediated by bFGF signaling and its possible crosstalk with prostate-specific membrane antigen (PSMA) in LNCaP and PC3-PSMA prostate cancer cell lines. PC3 cells stably transfected with PSMA gene were used for restoring PSMA expression. LNCaP and PC3-PSMA cells were exposed to 10 ng/mL of basic fibroblast growth factor (bFGF). IL-6 production was measured by ELISA assay, and levels of PSMA expression were assessed by flow cytometry. AKT, ERK1/2, and p38 phosphorylation were detected by Western blot. bFGF enhances IL-6 production in LNCaP and PC3-PSMA prostate cancer cells. The effect of bFGF on stimulating IL-6 secretion was greater in LNCaP than in PC3-PSMA cells. In the presence of bFGF, PSMA expression was activated after 4 days of treatment in LNCaP and PC3-PSMA cells. This activation was not maintained after long term of treatment in both metastatic cell lines. Solely MAPKs pathways (ERK1/2 and p38) were activated after bFGF stimulation in both metastatic cell lines, whereas AKT did not show any activation. The interference of the proinflammatory cytokine, IL-6, with bFGF signaling and PSMA, should be of high clinical relevance in the treatment of metastatic prostate cancer. In developing novel therapeutic modalities targeting IL-6, significant attention should be given to PSMA and its inactivation to fight against prostate cancer.
引用
收藏
页码:643 / 650
页数:8
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