Their increased metastatic potential and elevated IL-8 expression suggest a novel strategy for future therapeutic interventions to prevent osteosarcoma progression and metastasis.
The present study might lead not only to the clarification of a new molecular mechanism of invasion and metastasis of OS, but also to the development of a new therapeutic strategy of blocking IL-8 in OS.
By screening the expression of cytokines involved in the progression of OS, we found that activation of GPER can inhibit the expression of interleukin-6 (IL-6) and IL-8 in OS cells.
These results identify IL-6 and CXCL8 as primary mediators of OS lung tropism and suggest pleiotropic, redundant mechanisms by which they might effect metastasis.
Histone deacetylase 6 regulated expression of IL-8 is involved in the doxorubicin (Dox) resistance of osteosarcoma cells via modulating ABCB1 transcription.
We found that serum concentrations of CXCL8 and vascular endothelial growth factor were elevated in osteosarcoma patients in comparison with those in NCs.
An increased expression of IL6 and IL8 were found only in normal stromal cells, but not in OS cells, and this was confirmed in tumor-associated stromal cells isolated from OS tissue.
Our results showed that the IL-8-251 A/T genotype was associated with increased risk for development and metastasis of osteosarcoma in Chinese Han population.
These data indicated that IL-1Ra, IL-6, IL-8, and TNF-α were associated with increased risk of OS, in which IL-8 and TNF-α may be further correlated with the progression of this disease.
We have previously reported that titanium particles stimulate the selective induction of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) chemokines in human osteoblast-like osteosarcoma cells.
Human granulocyte chemotactic protein 2 (GCP-2) has originally been isolated from cytokine-stimulated osteosarcoma cells as a chemokine coproduced in minute amounts together with interleukin 8.