Involvement of Macrophages in Proliferation of Prostate Cancer Cells Infected with Trichomonas vaginalis
2
조회
0
다운로드
1
인용
0
참고문헌
키워드
초록
Macrophages play a key role in chronic inflammation, and are the most abundant immune cells in the tumor microenvironment. We investigated whether an interaction between inflamed prostate cancer cells stimulated with Trichomonas vaginalis and macrophages stimulates the proliferation of the cancer cells. Conditioned medium was prepared from T. vaginalis-infected (TCM) and uninfected (CM) mouse prostate cancer (PCa) cell line (TRAMP-C2 cells). Thereafter conditioned medium was prepared from macrophages (J774A.1 cell line) after incubation with CM (MCM) or TCM (MTCM). When TRAMP-C2 cells were stimulated with T. vaginalis, protein and mRNA levels of CXCL1 and CCL2 increased, and migration of macrophages toward TCM was more extensive than towards CM. Macrophages stimulated with TCM produced higher levels of CCL2, IL-6, TNF-α, their mRNAs than macrophages stimulated with CM. MTCM stimulated the proliferation and invasiveness of TRAMP-C2 cells as well as the expression of cytokine receptors (CCR2, GP130, CXCR2). Importantly, blocking of each cytokine receptors with anti-cytokine receptor antibody significantly reduced the proliferation and invasiveness of TRAMP-C2 cells. We conclude that inflammatory mediators released by TRAMP-C2 cells in response to infection by T. vaginalis stimulate the migration and activation of macrophages and the activated macrophages stimulate the proliferation and invasiveness of the TRAMP-C2 cells via cytokine-cytokine receptor binding. Our results therefore suggested that m
Abstract
Macrophages play a key role in chronic inflammation, and are the most abundant immune cells in the tumor microenvironment. We investigated whether an interaction between inflamed prostate cancer cells stimulated with Trichomonas vaginalis and macrophages stimulates the proliferation of the cancer cells. Conditioned medium was prepared from T. vaginalis-infected (TCM) and uninfected (CM) mouse prostate cancer (PCa) cell line (TRAMP-C2 cells). Thereafter conditioned medium was prepared from macrophages (J774A.1 cell line) after incubation with CM (MCM) or TCM (MTCM). When TRAMP-C2 cells were stimulated with T. vaginalis, protein and mRNA levels of CXCL1 and CCL2 increased, and migration of macrophages toward TCM was more extensive than towards CM. Macrophages stimulated with TCM produced higher levels of CCL2, IL-6, TNF-α, their mRNAs than macrophages stimulated with CM. MTCM stimulated the proliferation and invasiveness of TRAMP-C2 cells as well as the expression of cytokine receptors (CCR2, GP130, CXCR2). Importantly, blocking of each cytokine receptors with anti-cytokine receptor antibody significantly reduced the proliferation and invasiveness of TRAMP-C2 cells. We conclude that inflammatory mediators released by TRAMP-C2 cells in response to infection by T. vaginalis stimulate the migration and activation of macrophages and the activated macrophages stimulate the proliferation and invasiveness of the TRAMP-C2 cells via cytokine-cytokine receptor binding. Our results therefore suggested that m
참고문헌 (29)
- Conrad MD, "Extensive genetic diversity, unique population structure and evidence of genetic exchange in the sexually transmitted parasite Trichomonas vaginalis", PLoS Negl Trop Dis, 6, pp.e1573~ (2012)[DOI]
- Chetty R, "Genotypic variation in Trichomonas vaginalis detected in South African pregnant women", Infect Dis Obstet Gynecol, 2020, pp.1687427~ (2020)[DOI]
- Abdolrasouli A, "Persistent urethritis and prostatitis due to Trichomonas vaginalis: a case report", Can J Infect Dis Med Microbiol, 18, pp.308~310 (2007)[DOI]
- Sutcliffe S, "Trichomonosis, a common curable STI, and prostate carcinogenesis - a proposed molecular mechanism", PLoS Pathog, 8, pp.1002801~ (2012)[DOI]
- Gardner WA Jr, "Trichomonas vaginalis in the prostate gland", Arch Pathol Lab Med, 110, pp.430~432 (1986)
- 김정현, "Comparison of Seropositivity to Trichomonas vaginalis between Men with Prostatic Tumor and Normal Men", The Korean Journal of Parasitology, 57(1), pp.21~25 (2019), 대한기생충학ㆍ열대의학회[DOI]
- Adekoya TO, "Cytokines and chemokines as mediators of prostate cancer metastasis", Int J Mol Sci, 21, pp.4449~ (2020)[DOI]
- 김상수, "Proliferation of Mouse Prostate Cancer Cells Inflamed by Trichomonas vaginalis", The Korean Journal of Parasitology, 59(6), pp.547~556 (2021), 대한기생충학ㆍ열대의학회[DOI]
- Schoppmann SF, "Tumor-associated macrophages express lymphatic endothelial growth factors and are related to peritumoral lymphangiogenesis", Am J Pathol, 161, pp.947~956 (2002)[DOI]
- Lissbrant IF, "Tumor associated macrophages in human prostate cancer: relation to clinicopathological variables and survival", Int J Oncol, 17, pp.445~451 (2000)[DOI]
- 정효영, "Polarization of M2 Macrophages by Interaction between Prostate Cancer Cells Treated with Trichomonas vaginalis and Adipocytes", The Korean Journal of Parasitology, 58(3), pp.217~227 (2020), 대한기생충학ㆍ열대의학회[DOI]
- 김정현, "Signaling Role of Adipocyte Leptin in Prostate Cell Proliferation Induced by Trichomonas vaginalis", The Korean Journal of Parasitology, 59(3), pp.235~249 (2021), 대한기생충학ㆍ열대의학회[DOI]
- Han IH, "IL-6 produced by prostate epithelial cells stimulated with Trichomonas vaginalis promotes proliferation of prostate cancer cells by inducing M2 polarization of THP-1-derived macrophages", PLoS Negl Trop Dis, 14, pp.e0008126~ (2020)[DOI]
- Gordon S, "Monocyte and macrophage heterogeneity", Nat Rev Immunol, 5, pp.953~964 (2005)[DOI]
- Ginhoux F, "Tissue-resident macrophage ontogeny and homeostasis", Immunity, 44, pp.439~449 (2016)[DOI]
- Locati M, "Diversity, mechanisms and significance of macrophage plasticity", Annu Rev Pathol, 15, pp.123~147 (2020)[DOI]
- Mantovani A, "Tumorassociated macrophages as treatment targets in oncology", Nat Rev Clin Oncol, 14, pp.399~416 (2017)[DOI]
- Noy R, "Tumor-associated macrophages: from mechanisms to therapy", Immunity, 41, pp.49~61 (2014)[DOI]
- Dranoff G, "Cytokines in cancer pathogenesis and cancer therapy", Nat Rev Cancer, 4, pp.11~22 (2004)[DOI]
- Chow MT, "Chemokines in cancer", Cancer Immunol Res, 2, pp.1125~1131 (2014)[DOI]
- Nagarsheth N, "Chemokines in the cancer microenvironment and their relevance in cancer immunotherapy", Nat Rev Immunol, 17, pp.559~572 (2017)[DOI]
- Lu Y, "Monocyte chemotactic protein-1 (MCP-1) acts as a paracrine and autocrine factor for prostate cancer growth and invasion", Prostate, 66, pp.1311~1318 (2006)[DOI]
- Lu Y, "Activation of MCP-1", CCR2 axis promotes prostate cancer growth in bone, 2009, pp.26, 161~169
- Loberg RD, "CCL2 is a potent regulator of prostate cancer cell migration and proliferation", Neoplasia, 8, pp.578~586 (2006)[DOI]
- Han IH, "Signalling pathways associated with IL-6 production and epithelial-mesenchymal transition induction in prostate epithelial cells stimulated with Trichomonas vaginalis", Parasite Immunol, 38, pp.678~687 (2016)[DOI]
- Miyake M, "Chemokine (C-X-C motif) ligand 1 (CXCL1) protein expression is in-creased in high-grade prostate cancer", Pathol Res Pract, 210, pp.74~78 (2014)[DOI]
- Kuo PL, "CXCL1", GROα increases cell migration and invasion of prostate cancer by decreasing fibulin-1expression through NF-κB, Carcinogenesis, pp.2012, 33[DOI]
- Yongning Lu, "CXCL1-LCN2 paracrine axis promotes progression of prostate cancer via the Src activation and epithelial-mesenchymal transition", Cell Communication and Signaling, 17(1) (2019), Springer Science and Business Media LLC[DOI]
- Hardaway AL, "Marrow adipocyte-derived CXCL1 and CXCL2 contribute to osteolysis in metastatic prostate cancer", Clin Exp Metastasis, 32, pp.353~368 (2015)[DOI]