Interleukin-8 promotes prostate cancer bone metastasis through upregulation of bone sialoprotein.

Abstract

The aim of the present study was to investigate whether interleukin-8 (IL-8) enhances the ability of prostate cancer bone metastasis by influencing the coding level of bone sialoprotein (BSP). Cultured prostate cancer cell lines LNCaP (androgen dependent) and DU145 (androgen independent) were divided into three groups: IL-8 treatment group; IL-8 receptor inhibitor (SB225002) treatment group; and control group. Western blotting and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) were used to detect BSP protein and mRNA expression levels. Matrigel and bone adhesion experiments were used to detect the invasiveness of cancer cells and bone adhesion changes. Compared with the control group, western blotting and RT-qPCR results indicated that BSP protein and mRNA levels in LNCaP and DU145 were significantly upregulated following IL-8 treatment. Matrigel experiments indicated that following IL-8 treatment, the invasiveness of LNCaP and DU145 cells was significantly increased. The results of bone adhesion experiments indicated that following IL-8 treatment, the number of DU145 cells adhered to the surface of the bone was increased, compared with the control group. Following treatment of both cell lines with SB225002, western blotting and RT-qPCR results indicated that the expression levels of BSP protein and mRNA were significantly downregulated. Matrigel experiments indicated that following SB225002 treatment, the invasiveness of LNCaP and DU145 cells was significantly reduced. The number of DU145 cells adhered to the surface of the bone was reduced, compared with the untreated group. Therefore, IL-8 may promote prostate cancer bone metastasis by enhancing BSP regulation.