| Autor: |
Kim SS; Department of Environmental Biology and Medical Parasitology, Hanyang University College of Medicine, Seoul 04763, Korea.; Department of Biomedical Science, Hanyang University Graduate School of Biomedical Science and Engineering, Seoul 04763, Korea., Kim KS; Department of Urology, Hanyang University Guri Hospital, Hanyang University College of Medicine, Guri 11923, Korea., Han IH; Department of Environmental Biology and Medical Parasitology, Hanyang University College of Medicine, Seoul 04763, Korea.; Department of Biomedical Science, Hanyang University Graduate School of Biomedical Science and Engineering, Seoul 04763, Korea., Kim Y; Department of Pathology, Hanyang University College of Medicine, Seoul 04763, Korea., Bang SS; Department of Pathology, Hanyang University College of Medicine, Seoul 04763, Korea., Kim JH; Department of Environmental Biology and Medical Parasitology, Hanyang University College of Medicine, Seoul 04763, Korea.; Department of Biomedical Science, Hanyang University Graduate School of Biomedical Science and Engineering, Seoul 04763, Korea., Kim YS; Department of Biochemistry and Molecular Biology, Hanyang University College of Medicine, Seoul 04763, Korea., Choi SY; Department of Environmental Biology and Medical Parasitology, Hanyang University College of Medicine, Seoul 04763, Korea., Ryu JS; Department of Environmental Biology and Medical Parasitology, Hanyang University College of Medicine, Seoul 04763, Korea.; Department of Biomedical Science, Hanyang University Graduate School of Biomedical Science and Engineering, Seoul 04763, Korea. |
| Abstrakt: |
Our objective was to investigate whether inflammatory microenvironment induced by Trichomonas vaginalis infection can stimulate proliferation of prostate cancer (PCa) cells in vitro and in vivo mouse experiments. The production of CXCL1 and CCL2 increased when cells of the mouse PCa cells (TRAMP-C2 cell line) were infected with live T. vaginalis. T. vaginalis-conditioned medium (TCM) prepared from co-culture of PCa cells and T. vaginalis increased PCa cells migration, proliferation and invasion. The cytokine receptors (CXCR2, CCR2, gp130) were expressed higher on the PCa cells treated with TCM. Pretreatment of PCa cells with antibodies to these cytokine receptors significantly reduced the proliferation, mobility and invasiveness of PCa cells, indicating that TCM has its effect through cytokine-cytokine receptor signaling. In C57BL/6 mice, the prostates injected with T. vaginalis mixed PCa cells were larger than those injected with PCa cells alone after 4 weeks. Expression of epithelial-mesenchymal transition markers and cyclin D1 in the prostate tissue injected with T. vaginalis mixed PCa cells increased than those of PCa cells alone. Collectively, it was suggested that inflammatory reactions by T. vaginalis-stimulated PCa cells increase the proliferation and invasion of PCa cells through cytokine-cytokine receptor signaling pathways. |
