Inflammation

, Volume 36, Issue 3, pp 643–650

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

  • Awatef Ben Jemaa
  • Sataa Sallami
  • Dunia Ramarli
  • Marco Colombatti
  • Ridha Oueslati
Article

DOI: 10.1007/s10753-012-9586-7

Cite this article as:
Ben Jemaa, A., Sallami, S., Ramarli, D. et al. Inflammation (2013) 36: 643. doi:10.1007/s10753-012-9586-7

Abstract

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.

KEY WORDS

proinflammatory cytokineIL-6bFGFPSMAMAPKsAKTangiogenesisprostate cancer

Copyright information

© Springer Science+Business Media New York 2012

Authors and Affiliations

  • Awatef Ben Jemaa
    • 1
  • Sataa Sallami
    • 2
  • Dunia Ramarli
    • 3
  • Marco Colombatti
    • 3
  • Ridha Oueslati
    • 1
  1. 1.Unit of Immunology and Microbiology Environmental and Carcinogenesis (IMEC), Faculty of Sciences of BizerteUniversity of CarthageBizerteTunisia
  2. 2.Department of UrologyHospital of La Rabta TunisTunisTunisia
  3. 3.Clinical ImmunologyGiovanni Battista Rossi HospitalVeronaItaly