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Article ; Online: Fibroblast growth factor 2 suppresses the expression of C-C motif chemokine 11 through the c-Jun N-terminal kinase pathway in human dental pulp-derived mesenchymal stem cells.

Kurogoushi, Rika / Hasegawa, Tomokazu / Akazawa, Yuki / Iwata, Kokoro / Sugimoto, Asuna / Yamaguchi-Ueda, Kimiko / Miyazaki, Aya / Narwidina, Anrizandy / Kawarabayashi, Keita / Kitamura, Takamasa / Nakagawa, Hiroshi / Iwasaki, Tomonori / Iwamoto, Tsutomu

Experimental and therapeutic medicine

2021 Volume 22, Issue 6, Page(s) 1356

Abstract: ... and c-Jun N-terminal kinases (JNK) in SDP11 cells. The mechanism of the FGFR-downstream ...

Abstract	The regulation of the mesenchymal stem cell (MSC) programming mechanism promises great success in regenerative medicine. Tissue regeneration has been associated not only with the differentiation of MSCs, but also with the microenvironment of the stem cell niche that involves various cytokines and immune cells in the tissue regeneration site. In the present study, fibroblast growth factor 2 (FGF2), the principal growth factor for tooth development, dental pulp homeostasis and dentin repair, was reported to affect the expression of cytokines in human dental pulp-derived MSCs. FGF2 significantly inhibited the expression of chemokine C-C motif ligand 11 (CCL11) in a time- and dose-dependent manner in the SDP11 human dental pulp-derived MSC line. This inhibition was diminished following treatment with the AZD4547 FGF receptor (FGFR) inhibitor, indicating that FGF2 negatively regulated the expression of CCL11 in SDP11 cells. Furthermore, FGF2 activated the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK), extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun N-terminal kinases (JNK) in SDP11 cells. The mechanism of the FGFR-downstream signaling pathway was then studied using the SB203580, U0126 and SP600125 inhibitors for p38 MAPK, ERK1/2, and JNK, respectively. Interestingly, only treatment with SP600125 blocked the FGF2-mediated suppression of CCL11. The present results suggested that FGF2 regulated the expression of cytokines and suppressed the expression of CCL11 via the JNK signaling pathway in human dental pulp-derived MSCs. The present findings could provide important insights into the association of FGF2 and CCL11 in dental tissue regeneration therapy.
Language	English
Publishing date	2021-09-24
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2683844-8
ISSN	1792-1015 ; 1792-0981
ISSN (online)	1792-1015
ISSN	1792-0981
DOI	10.3892/etm.2021.10791
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Low dose hydroxylated PCB induces c-Jun expression in PC12 cells.

Shimokawa, Noriaki / Miyazaki, Wataru / Iwasaki, Toshiharu / Koibuchi, Noriyuki

Neurotoxicology

2006 Volume 27, Issue 2, Page(s) 176–183

Abstract: ... of gene expression and signal transduction. On the other hand, c-Jun, a component of AP-1, is likely to coordinate ... of PCBs on c-Jun expression. Here we investigated the expression of c-Jun in response to PCB. PC12 cells ... concentration from 10(-8) to 10(-5)M. The level of c-Jun expression was increased by OH-PCB at relatively low ...

Abstract	Polychlorinated biphenyls (PCBs) are known as environmental pollutants that may cause adverse health problems. Recently, accumulating evidence shows that PCBs express neurotoxicity through alteration of gene expression and signal transduction. On the other hand, c-Jun, a component of AP-1, is likely to coordinate transcription programs in response to various extracellular signals. However, little is known about the effects of PCBs on c-Jun expression. Here we investigated the expression of c-Jun in response to PCB. PC12 cells were incubated with hydroxylated PCB (4(OH)-2',3,3',4',5'-penta chlorobiphenyl, OH-PCB) at a final concentration from 10(-8) to 10(-5)M. The level of c-Jun expression was increased by OH-PCB at relatively low-dose; concentration of OH-PCB at 10(-8)M and 10(-7)M produced a 2.4- and 3.5-fold increase of c-Jun expression in respectively, compared with the values without OH-PCB treatment. Thyroid hormone (T3) did not induce such c-Jun expression, indicating that the effect of OH-PCB is not mediated through thyroid hormone signaling pathway. OH-PCB also enhanced phosphorylation of c-Jun NH2-terminal kinases. To determine whether the activation of Ca2+ channel is involved in the OH-PCB-induced c-Jun expression, we examined it using a L-type voltage-gated Ca2+ channel blocker nimodipine. Nimodipine partially inhibited OH-PCB-induced c-Jun expression by 50%. Moreover, Na+ channel antagonist tetrodotoxin inhibited OH-PCB-induced c-Jun expression completely. Taken together, our results indicate that exposure to OH-PCB induces c-Jun expression, and the response may be triggered by depolarization of a plasma membrane via Na+ influx, followed by Ca2+ influx partially through voltage-gated Ca2+ channels.
MeSH term(s)	Animals ; Blotting, Western ; Calcium/metabolism ; Calcium Channel Blockers/pharmacology ; Calcium Channels, L-Type/drug effects ; Calcium Channels, L-Type/metabolism ; Environmental Pollutants/toxicity ; Hydroxylation ; Indicators and Reagents ; MAP Kinase Kinase 4/biosynthesis ; MAP Kinase Kinase 4/genetics ; PC12 Cells ; Phosphorylation ; Polychlorinated Biphenyls/toxicity ; Proto-Oncogene Proteins c-jun/biosynthesis ; Rats ; Signal Transduction/drug effects ; Sodium Channels/drug effects ; Tetrodotoxin/pharmacology ; Thyroid Hormones/pharmacology ; Transcription Factor AP-1/drug effects ; Transcription Factor AP-1/physiology
Chemical Substances	Calcium Channel Blockers ; Calcium Channels, L-Type ; Environmental Pollutants ; Indicators and Reagents ; Proto-Oncogene Proteins c-jun ; Sodium Channels ; Thyroid Hormones ; Transcription Factor AP-1 ; Tetrodotoxin (4368-28-9) ; Polychlorinated Biphenyls (DFC2HB4I0K) ; MAP Kinase Kinase 4 (EC 2.7.12.2) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2006-03
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	800820-6
ISSN	0161-813X
ISSN	0161-813X
DOI	10.1016/j.neuro.2005.09.005
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Zs.A 1547: Show issues

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Article ; Online: PKCη promotes a proliferation to differentiation switch in keratinocytes via upregulation of p27Kip1 mRNA through suppression of JNK/c-Jun signaling under stress conditions.

Hara, T / Miyazaki, M / Hakuno, F / Takahashi, S / Chida, K

Cell death & disease

2011 Volume 2, Page(s) e157

Abstract: ... p27(Kip1) mRNA was downregulated, whereas JNK/c-Jun signaling was enhanced. Furthermore, inhibition ... of JNK/c-Jun signaling in PKCη-null keratinocytes led to upregulation of p27(Kip1) mRNA, and to thinner ... through suppression of JNK/c-Jun signaling. This results in promoting a proliferation to differentiation switch ...

Abstract	To maintain epidermal homeostasis, the balance between keratinocyte proliferation and differentiation is tightly controlled. However, the molecular mechanisms underlying this balance remain unclear. In 3D organotypic coculture with mouse keratinocytes and fibroblasts, the thickness of stratified cell layers was prolonged, and growth arrest and terminal differentiation were delayed when PKCη-null keratinocytes were used. Re-expression of PKCη in PKCη-null keratinocytes restored stratified cell layer thickness, growth arrest and terminal differentiation. We show that in 3D cocultured PKCη-null keratinocytes, p27(Kip1) mRNA was downregulated, whereas JNK/c-Jun signaling was enhanced. Furthermore, inhibition of JNK/c-Jun signaling in PKCη-null keratinocytes led to upregulation of p27(Kip1) mRNA, and to thinner stratified cell layers. Collectively, our findings indicate that PKCη upregulates p27(Kip1) mRNA through suppression of JNK/c-Jun signaling. This results in promoting a proliferation to differentiation switch in keratinocytes.
MeSH term(s)	Adenoviridae ; Animals ; Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; Coculture Techniques ; Cyclin-Dependent Kinase Inhibitor p27/genetics ; Cyclin-Dependent Kinase Inhibitor p27/metabolism ; Down-Regulation ; Epidermal Cells ; Epidermis/metabolism ; Fibroblasts/cytology ; Fibroblasts/metabolism ; HEK293 Cells ; Humans ; JNK Mitogen-Activated Protein Kinases/genetics ; JNK Mitogen-Activated Protein Kinases/metabolism ; Keratinocytes/cytology ; Keratinocytes/metabolism ; Mice ; Mice, Knockout ; Mitogen-Activated Protein Kinase 8/genetics ; Mitogen-Activated Protein Kinase 8/metabolism ; Protein Kinase C/genetics ; Protein Kinase C/metabolism ; RNA, Messenger/analysis ; RNA, Messenger/biosynthesis ; Signal Transduction ; Stress, Physiological ; Transfection ; Up-Regulation
Chemical Substances	RNA, Messenger ; Cyclin-Dependent Kinase Inhibitor p27 (147604-94-2) ; protein kinase C eta (EC 2.7.1.-) ; Protein Kinase C (EC 2.7.11.13) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 8 (EC 2.7.11.24)
Language	English
Publishing date	2011-05-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/cddis.2011.40
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Article: Adiponectin activates c-Jun NH2-terminal kinase and inhibits signal transducer and activator of transcription 3.

Miyazaki, Toshiaki / Bub, Jeffrey D / Uzuki, Miwa / Iwamoto, Yoshiki

Biochemical and biophysical research communications

2005 Volume 333, Issue 1, Page(s) 79–87

Abstract: ... of downstream signaling pathways. Here we identify c-Jun NH(2)-terminal kinase (JNK), and signal transducer and ...

Abstract	Adiponectin, a major adipose cytokine, plays a crucial role in the inhibition of metabolic syndrome by acting on such cell types as muscle cells and hepatocytes. Furthermore, evidence suggests that adiponectin may influence cancer pathogenesis. Adiponectin occurs in non-proteolytic (full-length adiponectin: f-adiponectin) and proteolytic (globular adiponectin: g-adiponectin) forms in various oligomeric states. Different forms of adiponectin show distinct biological effects through differential activation of downstream signaling pathways. Here we identify c-Jun NH(2)-terminal kinase (JNK), and signal transducer and activator of transcription 3 (STAT3) as common downstream effectors of f- and g-adiponectin. f- and g-adiponectin both stimulate JNK activation in prostate cancer DU145, PC-3, and LNCaP-FGC cells, hepatocellular carcinoma HepG2 cells, and C2C12 myoblasts. Furthermore, both f- and g-adiponectin drastically suppress constitutive STAT3 activation in DU145 and HepG2 cells. These suggest that JNK and STAT3 may constitute a universal signaling pathway to mediate adiponectin's pathophysiological effects on metabolic syndrome and cancer.
MeSH term(s)	Adiponectin ; Animals ; Cells, Cultured ; DNA-Binding Proteins/metabolism ; Enzyme Activation ; Gene Expression Regulation, Neoplastic ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; JNK Mitogen-Activated Protein Kinases/metabolism ; Myoblasts/metabolism ; Neoplasms/metabolism ; STAT3 Transcription Factor ; Signal Transduction ; Trans-Activators/metabolism
Chemical Substances	Adiponectin ; DNA-Binding Proteins ; Intercellular Signaling Peptides and Proteins ; STAT3 Transcription Factor ; STAT3 protein, human ; Trans-Activators ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2005-07-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2005.05.076
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Zs.A 116: Show issues

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Article ; Online: Effects of dominant-negative c-Jun on platelet-derived growth factor-induced vascular smooth muscle cell proliferation.

Zhan, Yumei / Kim, Shokei / Yasumoto, Hideo / Namba, Masashi / Miyazaki, Hitoshi / Iwao, Hiroshi

Arteriosclerosis, thrombosis, and vascular biology

2002 Volume 22, Issue 1, Page(s) 82–88

Abstract: ... This study was undertaken to examine the role of c-Jun in PDGF-BB-induced proliferation of rat aortic SMCs ... with recombinant adenovirus containing TAM67, a dominant-negative c-Jun lacking the transactivation domain of wild ... c-Jun (Ad-DN-c-Jun), to inhibit endogenous AP-1. Ad-DN-c-Jun, which specifically blocked AP-1 ...

Abstract	Although platelet-derived growth factor (PDGF)-BB is thought to participate in vascular disorders, the mechanism of PDGF-induced vascular smooth muscle cell (SMC) proliferation is not fully understood. This study was undertaken to examine the role of c-Jun in PDGF-BB-induced proliferation of rat aortic SMCs. PDGF-BB (10 ng/mL) significantly increased activator protein (AP)-1 DNA binding activity in SMCs, followed by the increase in [(3)H]thymidine incorporation and cell number. SMCs were infected with recombinant adenovirus containing TAM67, a dominant-negative c-Jun lacking the transactivation domain of wild c-Jun (Ad-DN-c-Jun), to inhibit endogenous AP-1. Ad-DN-c-Jun, which specifically blocked AP-1 transcriptional activity, significantly inhibited PDGF-BB-induced increases in [(3)H]thymidine incorporation or cell number. As shown by flow cytometric analysis, Ad-DN-c-Jun inhibited PDGF-BB-induced entrance of SMCs into S phase, leading to a G(1) arrest. Ad-DN-c-Jun attenuated PDGF-BB-induced downregulation of p27(Kip1), as shown by Western blot analysis, and the prevented PDGF-BB-induced decrease in cyclin E/cyclin-dependent kinase 2 complex-associated p27(Kip1), as shown by immunoprecipitation study. Furthermore, protein kinase assay showed that Ad-DN-c-Jun blocked PDGF-BB-induced activation of cyclin-dependent kinase 2. Our results provide the first evidence that dominant-negative c-Jun inhibits PDGF-BB-induced vascular SMC proliferation by preventing the downregulation of p27(Kip1), thereby supporting the important role of c-Jun in vascular SMC proliferation.
MeSH term(s)	Animals ; Becaplermin ; Cell Cycle Proteins/metabolism ; Cell Division ; G1 Phase ; Male ; Muscle, Smooth, Vascular/cytology ; Muscle, Smooth, Vascular/metabolism ; Mutation ; Platelet-Derived Growth Factor/metabolism ; Proto-Oncogene Proteins c-jun/genetics ; Proto-Oncogene Proteins c-jun/physiology ; Proto-Oncogene Proteins c-sis ; Rats ; Rats, Sprague-Dawley ; Receptors, Platelet-Derived Growth Factor/metabolism ; Transcription Factor AP-1/metabolism
Chemical Substances	Cell Cycle Proteins ; Platelet-Derived Growth Factor ; Proto-Oncogene Proteins c-jun ; Proto-Oncogene Proteins c-sis ; Transcription Factor AP-1 ; Becaplermin (1B56C968OA) ; Receptors, Platelet-Derived Growth Factor (EC 2.7.10.1)
Language	English
Publishing date	2002-01-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/hq0102.101821
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Zs.A 1705: Show issues

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Article: c-Jun NH(2)-terminal kinase mediates leptin-stimulated androgen-independent prostate cancer cell proliferation via signal transducer and activator of transcription 3 and Akt.

Miyazaki, Toshiaki / Bub, Jeffrey D / Iwamoto, Yoshiki

Biochimica et biophysica acta

2008 Volume 1782, Issue 10, Page(s) 593–604

Abstract: ... leptin stimulates androgen-independent prostate cancer cell proliferation through c-Jun NH(2)-terminal ...

Abstract	Obesity is associated with advanced prostate cancer. Here we demonstrate that in mouse prostate cancer TRAMP-C1 cells epididymal fat extracts from high-fat diet-fed obese mice stimulate androgen-independent cell growth more significantly than those from low-fat diet-fed lean mice or genetically obese leptin-deficient ob/ob mice in correlation with leptin concentrations. This result suggests that obesity promotes androgen-independent prostate cancer cell growth via adipose leptin. We have reported that added leptin stimulates androgen-independent prostate cancer cell proliferation through c-Jun NH(2)-terminal kinase (JNK). As with JNK, signal transducer and activator of transcription 3 (STAT3) and Akt are implicated in androgen-independent prostate cancer. In this study, we identify novel interaction of these three molecules in leptin-stimulated androgen-independent cell proliferation. Leptin activates JNK, STAT3 and Akt in a biphasic manner with a similar time-course. Pharmacological JNK inhibition suppresses leptin-stimulated DNA binding activity, as well as Ser-727 phosphorylation, of STAT3. Since JNK upregulates STAT3 activity via Ser-727 phosphorylation, JNK mediates leptin-stimulated STAT3 activation through Ser-727 phosphorylation. Moreover, JNK inhibition impairs leptin-stimulated Ser-473 phosphorylation of Akt that is required for its activation. Thus, JNK is involved in leptin-stimulated Akt activation. These findings together indicate that JNK mediates leptin-stimulated androgen-independent prostate cancer cell proliferation via STAT3 and Akt.
MeSH term(s)	Adipose Tissue, White/chemistry ; Animals ; Antibodies/pharmacology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; DNA/metabolism ; Enzyme Inhibitors/pharmacology ; Gene Expression/genetics ; Humans ; JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors ; JNK Mitogen-Activated Protein Kinases/metabolism ; Leptin/immunology ; Leptin/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Models, Biological ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors ; Phosphorylation/drug effects ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Protein Binding/drug effects ; Proto-Oncogene Proteins c-akt/metabolism ; Receptors, Leptin/genetics ; STAT3 Transcription Factor/metabolism ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Tissue Extracts/pharmacology
Chemical Substances	Antibodies ; Enzyme Inhibitors ; Leptin ; Receptors, Leptin ; STAT3 Transcription Factor ; Tissue Extracts ; DNA (9007-49-2) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2008-10
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2008.07.005
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Uc I Zs.247: Show issues

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Article: Dominant negative c-jun gene transfer inhibits vascular smooth muscle cell proliferation and neointimal hyperplasia in rats.

Yasumoto, H / Kim, S / Zhan, Y / Miyazaki, H / Hoshiga, M / Kaneda, Y / Morishita, R / Iwao, H

Gene therapy

2001 Volume 8, Issue 22, Page(s) 1682–1689

Abstract: We previously reported that activator protein-1 (AP-1), containing c-Jun, is rapidly activated ... in balloon-injured artery. Therefore, we examined the role of c-Jun in vascular smooth muscle cell (SMC ... a dominant negative c-Jun lacking transactivation domain of wild c-Jun (Ad-DN-c-Jun), to specifically inhibit ...

Abstract	We previously reported that activator protein-1 (AP-1), containing c-Jun, is rapidly activated in balloon-injured artery. Therefore, we examined the role of c-Jun in vascular smooth muscle cell (SMC) proliferation, by using in vitro and in vivo gene transfer techniques. (1) Serum (2%) stimulation significantly increased AP-1 DNA binding activity in aortic SMCs, followed by the increase in both 3H-thymidine incorporation and cell number. Aortic SMCs were infected with recombinant adenovirus containing TAM67, a dominant negative c-Jun lacking transactivation domain of wild c-Jun (Ad-DN-c-Jun), to specifically inhibit AP-1. Ad-DN-c-Jun significantly inhibited serum-induced SMC proliferation, by inhibiting the entrance of SMC into S phase. (2) The effect of DN-c-Jun was examined on balloon injury-induced intimal hyperplasia in rats. Before balloon injury, DN-c-Jun was transfected into rat carotid artery using the hemagglutinating virus of Japan-liposome method. In vivo transfection of DN-c-Jun significantly inhibited vascular SMC proliferation in the intima and the media and subsequently prevented intimal thickening at 14 days after balloon injury. We obtained the first evidence that DN-c-Jun gene transfer prevented vascular SMC proliferation in vitro and in vivo, and c-Jun was involved in balloon injury-induced intimal hyperplasia. Thus, AP-1 seems to be the new therapeutic target for treatment of vascular diseases.
MeSH term(s)	Animals ; Aorta ; Carotid Artery Injuries/pathology ; Carotid Artery Injuries/therapy ; Cell Division/genetics ; Gene Expression ; Genes, jun ; Genetic Therapy/methods ; Hyperplasia/genetics ; Male ; Muscle, Smooth, Vascular/metabolism ; Muscle, Smooth, Vascular/pathology ; Rats ; Rats, Sprague-Dawley ; Transcription Factor AP-1/metabolism ; Transfection/methods ; Tunica Intima/metabolism ; Tunica Intima/pathology
Chemical Substances	Transcription Factor AP-1
Language	English
Publishing date	2001-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1191036-7
ISSN	1476-5462 ; 0969-7128
ISSN (online)	1476-5462
ISSN	0969-7128
DOI	10.1038/sj.gt.3301590
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Zs.A 3991: Show issues

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Article: Adenovirus-mediated overexpression of REIC/Dkk-3 selectively induces apoptosis in human prostate cancer cells through activation of c-Jun-NH2-kinase.

Abarzua, Fernando / Sakaguchi, Masakiyo / Takaishi, Mikiro / Nasu, Yasutomo / Kurose, Kyouhei / Ebara, Shin / Miyazaki, Masahiro / Namba, Masayoshi / Kumon, Hiromi / Huh, Nam-ho

Cancer research

2005 Volume 65, Issue 21, Page(s) 9617–9622

Abstract: ... proficient normal prostate epithelial and stromal cells. The apoptosis involved c-Jun-NH2-kinase activation ...

Abstract	Alteration in genes which takes place during malignant conversion and progression could be potential targets for gene therapy. We previously identified REIC/Dkk-3 as a gene whose expression is reduced in many human cancers. Here, we showed that expression of REIC/Dkk-3 was consistently reduced in human prostate cancer tissues in a stage-dependent manner. Forced expression of REIC/Dkk-3 induced apoptosis in human prostate cancer cell lines lacking endogenous REIC/Dkk-3 expression but not in REIC/Dkk-3-proficient normal prostate epithelial and stromal cells. The apoptosis involved c-Jun-NH2-kinase activation, mitochondrial translocation of Bax, and reduction of Bcl-2. A single injection of an adenovirus vector carrying REIC/Dkk-3 showed a dramatic antitumor effect on a xenotransplanted human prostate cancer. Thus, REIC/Dkk-3 could be a novel target for gene-based therapy of prostate cancer.
MeSH term(s)	Adenoviridae/genetics ; Animals ; Apoptosis ; Cell Line, Tumor ; Enzyme Activation ; Genetic Therapy/methods ; Humans ; Intercellular Signaling Peptides and Proteins ; JNK Mitogen-Activated Protein Kinases/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Prostatic Neoplasms/therapy ; Proteins/antagonists & inhibitors ; Proteins/genetics ; Proteins/metabolism ; Xenograft Model Antitumor Assays
Chemical Substances	DKK3 protein, human ; Intercellular Signaling Peptides and Proteins ; Proteins ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2005-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-05-0829
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Uh III Zs.135/5: Show issues

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Article: Tacrolimus and cyclosporine A inhibit human osteoclast formation via targeting the calcineurin-dependent NFAT pathway and an activation pathway for c-Jun or MITF in rheumatoid arthritis.

Miyazaki, Masashi / Fujikawa, Yosuke / Takita, Chikahiro / Tsumura, Hiroshi

Clinical rheumatology

2007 Volume 26, Issue 2, Page(s) 231–239

Abstract: ... c-Fos, c-Jun, microphthalmia transcription factor (MITF) and PU.1 in mononuclear cells (MNCs) was ... of tacrolimus or cyclosporine A resulted in a decrease in the mRNA expression of NFATc1, c-Jun, and MITF ... via targeting both the calcineurin-dependent NFAT pathway and activation pathway for c-Jun or MITF. ...

Abstract	In the present study, we aimed to determine whether tacrolimus (FK506) and cyclosporine A act directly on human osteoclast precursors obtained from patients with rheumatoid arthritis (RA) and influence monocyte-osteoclast differentiation induced by receptor activator of NF-kappaB ligand (RANKL) in vitro, the stage at which differentiation was affected and the manner in which tacrolimus or cyclosporine A affected the osteoclast signaling pathway. Peripheral blood mononuclear cells (PBMCs) were isolated from RA patients and cultured in the presence of RANKL and macrophage-colony stimulating factor (M-CSF). Tacrolimus or cyclosporine A was added to these cultures to determine the effect on the osteoclast differentiation. Osteoclast formation was determined by assessing the number of tartrate resistant acid phosphatase (TRAP) staining cells and measuring the extent of lacunar resorption. The expression of osteoclast transcription factors, such as TNF receptor-associated factor 6 (TRAF6), nuclear factor of activated T cells c1 (NFATc1), c-Fos, c-Jun, microphthalmia transcription factor (MITF) and PU.1 in mononuclear cells (MNCs) was assayed by quantitative reverse transcription-polymerase chain reaction. Addition of tacrolimus or cyclosporine A resulted in a decrease in the number of TRAP-positive multinucleated cells (TRAP+ MNCs) and a decrease in the extent of lacunar resorption pit formation as compared to the control cultures; thus, human monocyte-osteoclast differentiation was more effectively inhibited at the late stage and addition of tacrolimus or cyclosporine A resulted in a decrease in the mRNA expression of NFATc1, c-Jun, and MITF at the late stage. Our results suggest that tacrolimus or cyclosporine A acts directly on human osteoclast precursors in RA patients and exerts their immunosuppressive effects on human monocyte-osteoclast formation via targeting both the calcineurin-dependent NFAT pathway and activation pathway for c-Jun or MITF.
MeSH term(s)	Adolescent ; Adult ; Aged ; Cell Count ; Cell Differentiation/drug effects ; Cell Survival/drug effects ; Cells, Cultured ; Cyclosporine/pharmacology ; Dose-Response Relationship, Drug ; Female ; Gene Expression/drug effects ; Humans ; Immunosuppressive Agents/pharmacology ; Leukocytes, Mononuclear/drug effects ; Leukocytes, Mononuclear/metabolism ; Leukocytes, Mononuclear/pathology ; Male ; Microphthalmia-Associated Transcription Factor/genetics ; Microphthalmia-Associated Transcription Factor/metabolism ; Middle Aged ; NFATC Transcription Factors/genetics ; NFATC Transcription Factors/metabolism ; Osteoclasts/drug effects ; Osteoclasts/metabolism ; Osteoclasts/pathology ; Proto-Oncogene Proteins c-jun/genetics ; Proto-Oncogene Proteins c-jun/metabolism ; RNA, Messenger/metabolism ; Tacrolimus/pharmacology
Chemical Substances	Immunosuppressive Agents ; MITF protein, human ; Microphthalmia-Associated Transcription Factor ; NFATC Transcription Factors ; NFATC1 protein, human ; Proto-Oncogene Proteins c-jun ; RNA, Messenger ; Cyclosporine (83HN0GTJ6D) ; Tacrolimus (WM0HAQ4WNM)
Language	English
Publishing date	2007-02
Publishing country	Germany
Document type	Journal Article
ZDB-ID	604755-5
ISSN	0770-3198
ISSN	0770-3198
DOI	10.1007/s10067-006-0287-1
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Article: Differential induction of fos and jun family genes by thyrotropin in rat thyroid FRTL-5 cells.

Kambe, F / Miyazaki, T / Seo, H

Thyroid : official journal of the American Thyroid Association

1996 Volume 6, Issue 2, Page(s) 123–128

Abstract: Effect of thyrotropin (TSH) on the expression of the members of fos and jun family genes in a rat ... TSH induced similar changes in the levels of c-jun and junB mRNAs. They significantly increased ... within 30 min followed by a sustained high level until 90 min. The differential induction of fos and jun ...

Abstract	Effect of thyrotropin (TSH) on the expression of the members of fos and jun family genes in a rat thyroid cell line (FRTL-5) was examined by the reverse transcription-polymerase chain reaction (RT-PCR) method. FRTL-5 cells were maintained in a TSH-deprived medium for 5 days. After 1 mU/mL TSH addition, the cells were harvested at intervals. Total RNA extracted from the cells was subjected to RT-PCR. TSH induced a rapid and transient expression of c-fos, fosB, and fra-1 with different kinetics. Increase in c-fos mRNA was most rapid with a peak level at 30 min after TSH addition. The fosB mRNA reached a peak level at 60 min poststimulation with a rapid decline at 90 min. The fra-1 mRNA increased at 60 min followed by a gradual decrease until 120 min. The change in fra-2 mRNA level was similar to that of fra-1. TSH induced similar changes in the levels of c-jun and junB mRNAs. They significantly increased within 30 min followed by a sustained high level until 90 min. The differential induction of fos and jun family genes suggests an important role of their gene products on the regulation of thyroid cell function by TSH.
MeSH term(s)	Animals ; Base Sequence ; Cell Line ; Gene Expression/drug effects ; Molecular Sequence Data ; Polymerase Chain Reaction ; Proto-Oncogene Proteins c-fos/biosynthesis ; Proto-Oncogene Proteins c-fos/genetics ; Proto-Oncogene Proteins c-jun/biosynthesis ; Proto-Oncogene Proteins c-jun/genetics ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; RNA, Messenger/isolation & purification ; Rats ; Thyroid Gland/drug effects ; Thyroid Gland/metabolism ; Thyrotropin/pharmacology
Chemical Substances	Proto-Oncogene Proteins c-fos ; Proto-Oncogene Proteins c-jun ; RNA, Messenger ; Thyrotropin (9002-71-5)
Language	English
Publishing date	1996-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1086044-7
ISSN	1557-9077 ; 1050-7256
ISSN (online)	1557-9077
ISSN	1050-7256
DOI	10.1089/thy.1996.6.123
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