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Title 

TLR7 expression is decreased during tumour progression in transgenic adenocarcinoma of mouse prostate mice and its activation inhibits growth of prostate cancer cells

Authors 

J H HanS Y ParkJ B KimS D ChoB KimBo Yeon KimM J KangD J KimJ H Park

Publisher 

Wiley-Blackwell

Issue Date 

2013

Citation 

American Journal of Reproductive Immunology, vol. 70, no. 4, pp. 317-326

Keywords 

Colony formationGrowth inhibitionProstate cancerTLR7Transgenic adenocarcinoma of mouse prostate mice

Abstract 

Problem: Although various Toll-like receptors (TLRs) have been associated with immune response and tumorigenesis in the prostate cells, little is known about the role of TLR7. Accordingly, we examined the expression of TLR7 during tumour progression of TRMAP (transgenic mouse model for prostate cancer) mice and its role on cell growth. Method of study: Toll-like receptor7 expression was examined by RT-polymerase chain reaction (PCR), Western blot, and immunohistochemistry. Cell growth was examined by MTT assay. Colony formation was investigated by crystal violet staining. Results: Strong expression of TLR7 was detected in the normal prostate epithelia of Wild-type (WT) mice, but not in TLR7-deficient mice. In contrast, TLR7 expression was weak in transgenic adenocarcinoma of mouse prostate (TRAMP)-C2 cells, as compared with murine bone marrow-derived macrophages (BMDMs). Moreover, TLR7 mRNA was markedly expressed in RWPE-1 cells (non-cancerous prostate epithelial cells), but not in PC3 and DU145 (prostate cancer cells). Immunohistochemically, TLR7 expression gradually decreased in TRAMP mice depending on the pathologic grade of the prostate cells. TLR7 agonists increased both the gene and protein expression of TLR7 and promoted production of proinflammatory cytokines/chemokines and IFN-β gene expression in prostate cancer cell lines. Moreover, loxoribine inhibited the growth and colony formation of TRAMP-C2 cells dependent of TLR7. Conclusion: These findings suggest that TLR7 may participate in tumour suppression in the prostate cells.

ISSN 

1046-7408

Link 

http://dx.doi.org/10.1111/aji.12146

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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