TLR7 Expression is Decreased During Tumour Progression in Transgenic Adenocarcinoma of Mouse Prostate Mice and Its Activation Inhibits Growth of Prostate Cancer Cells
Identifieur interne : 001150 ( Main/Exploration ); précédent : 001149; suivant : 001151TLR7 Expression is Decreased During Tumour Progression in Transgenic Adenocarcinoma of Mouse Prostate Mice and Its Activation Inhibits Growth of Prostate Cancer Cells
Auteurs : Ju-Hee Han [Corée du Sud] ; Shin-Young Park [Corée du Sud] ; Jin-Bum Kim [Corée du Sud] ; Sung-Dae Cho [Corée du Sud] ; Bumseok Kim [Corée du Sud] ; Bo-Yeon Kim [Corée du Sud] ; Min-Jung Kang [Corée du Sud] ; Dong-Jae Kim [Corée du Sud] ; Jae-Hak Park [Corée du Sud] ; Jong-Hwan Park [Corée du Sud]Source :
- American Journal of Reproductive Immunology [ 1046-7408 ] ; 2013-10.
English descriptors
- Teeft :
- Adenocarcinoma, Agonist, American journal, Assay, Cell growth, Chemokine production, Chloroquine, Colony formation, Crystal violet assay, Epithelial, Epithelium, Gene expression, Human prostate cancer cells, Imiquimod, Immune, Immune response, Immunol, Immunology, Independent experiments, John wiley sons, Konyang university, Loxoribine, Mouse, Mouse prostate, Mouse prostate mice, Mrna, Normal prostate epithelia, Positive control, Prostate, Prostate cancer, Prostate cancer cell lines, Prostate cancer cells, Prostate cells, Prostate epithelial cells, Prostatic, Protein expression, Receptor, Representative experiment, Reproductive, Reproductive immunology, Tlr4, Tlr7, Tlr7 agonists, Tlr7 expression, Tlr7 mrna, Tlr7 stimulation, Tlrs, Tramp, Tramp mice, Transgenic, Transgenic adenocarcinoma, Tumorigenesis, Tumour, Tumour progression, Veterinary medicine, Vivo study.
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.
Url:
DOI: 10.1111/aji.12146
Affiliations:
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first="Sung-Dae" last="Cho">Sung-Dae Cho</name><affiliation wicri:level="1"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Oral Pathology, School of Dentistry and Institute of Oral Bioscience, Brain Korea 21 Project, Chonbuk National University, Jeonju</wicri:regionArea><wicri:noRegion>Jeonju</wicri:noRegion></affiliation></author><author><name sortKey="Kim, Bumseok" sort="Kim, Bumseok" uniqKey="Kim B" first="Bumseok" last="Kim">Bumseok Kim</name><affiliation wicri:level="1"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Biosafety Research Institute and College of Veterinary Medicine, Chonbuk National University, Jeonju</wicri:regionArea><wicri:noRegion>Jeonju</wicri:noRegion></affiliation></author><author><name sortKey="Kim, Bo Eon" sort="Kim, Bo Eon" uniqKey="Kim B" first="Bo-Yeon" last="Kim">Bo-Yeon Kim</name><affiliation wicri:level="1"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>World Class Institute, Korea Research Institute of Bioscience and Biotechnology, Choongbuk</wicri:regionArea><wicri:noRegion>Choongbuk</wicri:noRegion></affiliation></author><author><name sortKey="Kang, Min Ung" sort="Kang, Min Ung" uniqKey="Kang M" first="Min-Jung" last="Kang">Min-Jung Kang</name><affiliation wicri:level="1"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Biochemistry, College of Medicine, Konyang University, Daejeon</wicri:regionArea><wicri:noRegion>Daejeon</wicri:noRegion></affiliation></author><author><name sortKey="Kim, Dong Ae" sort="Kim, Dong Ae" uniqKey="Kim D" first="Dong-Jae" last="Kim">Dong-Jae Kim</name><affiliation wicri:level="1"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Biochemistry, College of Medicine, Konyang University, Daejeon</wicri:regionArea><wicri:noRegion>Daejeon</wicri:noRegion></affiliation></author><author><name sortKey="Park, Jae Ak" sort="Park, Jae Ak" uniqKey="Park J" first="Jae-Hak" last="Park">Jae-Hak 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Konyang University, Daejeon</wicri:regionArea><wicri:noRegion>Daejeon</wicri:noRegion></affiliation><affiliation></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Corée du Sud</country></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">American Journal of Reproductive Immunology</title><title level="j" type="alt">AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY</title><idno type="ISSN">1046-7408</idno><idno type="eISSN">1600-0897</idno><imprint><biblScope unit="vol">70</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="317">317</biblScope><biblScope unit="page" to="326">326</biblScope><biblScope unit="page-count">10</biblScope><date type="published" when="2013-10">2013-10</date></imprint><idno type="ISSN">1046-7408</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1046-7408</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Adenocarcinoma</term><term>Agonist</term><term>American journal</term><term>Assay</term><term>Cell growth</term><term>Chemokine production</term><term>Chloroquine</term><term>Colony formation</term><term>Crystal violet assay</term><term>Epithelial</term><term>Epithelium</term><term>Gene expression</term><term>Human prostate cancer cells</term><term>Imiquimod</term><term>Immune</term><term>Immune response</term><term>Immunol</term><term>Immunology</term><term>Independent experiments</term><term>John wiley sons</term><term>Konyang university</term><term>Loxoribine</term><term>Mouse</term><term>Mouse prostate</term><term>Mouse prostate mice</term><term>Mrna</term><term>Normal prostate epithelia</term><term>Positive control</term><term>Prostate</term><term>Prostate cancer</term><term>Prostate cancer cell lines</term><term>Prostate cancer cells</term><term>Prostate cells</term><term>Prostate epithelial cells</term><term>Prostatic</term><term>Protein expression</term><term>Receptor</term><term>Representative experiment</term><term>Reproductive</term><term>Reproductive immunology</term><term>Tlr4</term><term>Tlr7</term><term>Tlr7 agonists</term><term>Tlr7 expression</term><term>Tlr7 mrna</term><term>Tlr7 stimulation</term><term>Tlrs</term><term>Tramp</term><term>Tramp mice</term><term>Transgenic</term><term>Transgenic adenocarcinoma</term><term>Tumorigenesis</term><term>Tumour</term><term>Tumour progression</term><term>Veterinary medicine</term><term>Vivo study</term></keywords></textClass></profileDesc></teiHeader><front><div type="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.</div></front></TEI><affiliations><list><country><li>Corée du Sud</li></country><region><li>Région capitale de Séoul</li></region><settlement><li>Séoul</li></settlement></list><tree><country name="Corée du Sud"><region name="Région capitale de Séoul"><name sortKey="Han, Ju Ee" sort="Han, Ju Ee" uniqKey="Han J" first="Ju-Hee" last="Han">Ju-Hee Han</name></region><name sortKey="Cho, Sung Ae" sort="Cho, Sung Ae" uniqKey="Cho S" first="Sung-Dae" last="Cho">Sung-Dae Cho</name><name sortKey="Kang, Min Ung" sort="Kang, Min Ung" uniqKey="Kang M" first="Min-Jung" last="Kang">Min-Jung Kang</name><name sortKey="Kim, Bo Eon" sort="Kim, Bo Eon" uniqKey="Kim B" first="Bo-Yeon" last="Kim">Bo-Yeon Kim</name><name sortKey="Kim, Bumseok" sort="Kim, Bumseok" uniqKey="Kim B" first="Bumseok" last="Kim">Bumseok Kim</name><name sortKey="Kim, Dong Ae" sort="Kim, Dong Ae" uniqKey="Kim D" first="Dong-Jae" last="Kim">Dong-Jae Kim</name><name sortKey="Kim, Jin Um" sort="Kim, Jin Um" uniqKey="Kim J" first="Jin-Bum" last="Kim">Jin-Bum Kim</name><name sortKey="Park, Jae Ak" sort="Park, Jae Ak" uniqKey="Park J" first="Jae-Hak" last="Park">Jae-Hak Park</name><name sortKey="Park, Jae Ak" sort="Park, Jae Ak" uniqKey="Park J" first="Jae-Hak" last="Park">Jae-Hak Park</name><name sortKey="Park, Jong Wan" sort="Park, Jong Wan" uniqKey="Park J" first="Jong-Hwan" last="Park">Jong-Hwan Park</name><name sortKey="Park, Jong Wan" sort="Park, Jong Wan" uniqKey="Park J" first="Jong-Hwan" last="Park">Jong-Hwan Park</name><name sortKey="Park, Jong Wan" sort="Park, Jong Wan" uniqKey="Park J" first="Jong-Hwan" last="Park">Jong-Hwan Park</name><name sortKey="Park, Shin Oung" sort="Park, Shin Oung" uniqKey="Park S" first="Shin-Young" last="Park">Shin-Young Park</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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