研究者詳細 - 伊原木　聰一郎

論文 - 伊原木　聰一郎

分割表示 187 件中 161 - 180 件目／全件表示 >>

Bone destruction by invading oral squamous carcinoma cells mediated by the transforming growth factor-beta signalling pathway. 査読国際誌

Takeshi Goda, Tsuyoshi Shimo, Yasuto Yoshihama, Nur Mohammad Monsur Hassan, Soichiro Ibaragi, Naito Kurio, Tatsuo Okui, Tatsuki Honami, Koji Kishimoto, Akira Sasaki

Anticancer research 30 ( 7 ) 2615 - 23 2010年7月

記述言語：英語

BACKGROUND: Gingival squamous cell carcinoma (SCC) cells frequently invade mandibular bone, and this destruction is associated with a worse prognosis. However, the relationship between bone destruction and associated factors is unclear. In this study, the role and diagnostic utility of transforming growth factor-beta (TGF-beta) type I receptor (TbetaRI) in bone destruction of the mandible was investigated. PATIENTS AND METHODS: The expression of TbetaRI was explored by using an immunohistochemical method on paraffin-embedded tissues from 21 cases of mandibular SCC. An inhibitor of the kinase activity of the TbetaRI (TbetaRI-I) was used to assess the role of TbetaRI in bone destruction by a human oral SCC cell line (HSC-2) that highly expresses TbetaRI. RESULTS: TbetaRI-positive signals were closely associated with destructive invasion of the mandible by oral SCC cells. Consistent with these results, TbetaRI-I greatly reduced HSC-2 cell-induced bone destruction and osteoclast formation in vivo and in vitro. TbetaRI-I treatment reduced the expression of TNF-alpha, RANKL and connective tissue growth factor (CTGF/CCN2), all of which were up-regulated by TGF-beta in HSC-2 cells. CONCLUSION: These data demonstrated an important role for TGF-beta signalling in bone invasion by oral SCC cells, and suggest that the bone destruction is mediated by RANKL, TNF-alpha and CCN2.

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Novel transcriptional regulation of CCN2/CTGF by nuclear translocation of MMP3 査読

Takanori Eguchi, Satoshi Kubota, Kazumi Kawata, Yoshiki Mukudai, Junji Uehara, Toshihiro Ohgawara, Soichiro Ibaragi, Akira Sasaki, Takuo Kuboki, Masaharu Takigawa

CCN Proteins in Health and Disease: An Overview of the Fifth International Workshop on the CCN Family of Genes 255 - 264 2010年

当科におけるインプラント患者の臨床統計的検討

帆波辰基, 目瀬浩, 西山明慶, 岸本晃治, 塚本剛一, 志茂剛, 吉岡徳枝, 銅前昇平, 中妻加奈子, 辻本紗代子, 伊原木聰一郎, 佐々木朗

岡山歯学会雑誌 28 ( 2 ) 151 - 155 2009年12月

Epithelial-Mesenchymal Transition and Cell Cooperativity in Metastasis 査読国際誌

Takanori Tsuji, Soichiro Ibaragi, Guo-fu Hu

CANCER RESEARCH 69 ( 18 ) 7135 - 7139 2009年9月

当科における口腔扁平上皮癌の治療成績(第1報)

岸本晃治, 吉田祥子, 伊原木聰一郎, 銅前昇平, 吉岡徳枝, 志茂剛, 塚本剛一, 西山明慶, 目瀬浩, 松村智弘, 佐々木朗

岡山歯学会雑誌 28 ( 1 ) 43 - 50 2009年6月

Inactivation of AMPK alters gene expression and promotes growth of prostate cancer cells. 査読国際誌

J Zhou, W Huang, R Tao, S Ibaragi, F Lan, Y Ido, X Wu, Y O Alekseyev, M E Lenburg, G-f Hu, Z Luo

Oncogene 28 ( 18 ) 1993 - 2002 2009年5月

記述言語：英語

AMP-activated protein kinase (AMPK) serves as a fuel-sensing enzyme that is activated by binding of AMP and subsequent phophorylation by upstream kinases such as the tumor suppressor LKB1, when cells sense an increase in the ratio of AMP to ATP. Acute activation of AMPK stimulates fatty acid oxidation to generate more ATP and simultaneously inhibits ATP-consuming processes including fatty acid and protein syntheses, thereby preserving energy for acute cell-surviving program, whereas chronic activation leads to inhibition of cell growth. The goal of the present study is to explore the mechanisms by which AMPK regulates cell growth. Toward this end, we established stable cell lines by introducing a dominant-negative mutant of AMPK alpha1 subunit or its shRNA into the prostate cancer C4-2 cells and other cells, or wild type LKB1 into the lung adenocarcinoma A549 and breast MB-MDA-231 cancer cells, both of which lack functional LKB1. Our results showed that the inhibition of AMPK accelerated cell proliferation and promoted malignant behavior such as increased cell migration and anchorage-independent growth. This was associated with decreased G1 population, downregulation of p53 and p21, and upregulation of S6K, IGF-1 and IGF1R. Conversely, treatment of the C4-2 cells with 5-aminoimidazole-4-carboxamide 1-D-ribonucleoside (AICAR), a prototypical AMPK activator, caused opposite changes. In addition, our study using microarray and RT-PCR revealed that AMPK regulated gene expression involved in tumor cell growth and survival. Thus, our study provides novel insights into the mechanisms of AMPK action in cancer cells and presents AMPK as an ideal drug target for cancer therapy.

DOI： 10.1038/onc.2009.63

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われわれの施設における顎変形症治療の実態顎変形症学会2006年度全国調査と比較して

江藤司, 西山明慶, 吉岡徳枝, 伊原木聰一郎, 吉田祥子, 尾野裕子, 佐々木朗

日本顎変形症学会雑誌 19 ( 2 ) 121 - 121 2009年5月

Neamine inhibits prostate cancer growth by suppressing angiogenin-mediated rRNA transcription. 査読国際誌

Soichiro Ibaragi, Norie Yoshioka, Shuping Li, Miaofen G Hu, Saori Hirukawa, Peter M Sadow, Guo-Fu Hu

Clinical cancer research : an official journal of the American Association for Cancer Research 15 ( 6 ) 1981 - 8 2009年3月

記述言語：英語

PURPOSE: Angiogenin (ANG) undergoes nuclear translocation and stimulates rRNA transcription in both prostate cancer cells and endothelial cells. The purpose of this study is to assess the antitumor activity of neamine, a nontoxic degradation product of neomycin that blocks nuclear translocation of ANG. EXPERIMENTAL DESIGN: The anti-prostate cancer activity of neamine was first evaluated in a xenograft animal model. It was then examined in the murine prostate-restricted AKT transgenic mice that develop prostate intraepithelial neoplasia (PIN) owing to AKT transgene overexpression. RESULTS: Neamine inhibits xenograft growth of PC-3 human prostate cancer cells in athymic mice. It blocks nuclear translocation of ANG and inhibits rRNA transcription, cell proliferation, and angiogenesis. Neamine also prevents AKT-induced PIN formation as well as reverses fully developed PIN in murine prostate-restricted AKT mice, accompanied by a decrease in rRNA synthesis, cell proliferation, and angiogenesis and an increase in prostate epithelial cell apoptosis. CONCLUSION: We confirmed that ANG is a molecular target for cancer drug development and that blocking nuclear translocation of ANG is an effective means to inhibit its activity. Our results also suggested that neamine is a lead compound for further preclinical evaluation.

DOI： 10.1158/1078-0432.CCR-08-2593

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Angiogenin-stimulated rRNA transcription is essential for initiation and survival of AKT-induced prostate intraepithelial neoplasia. 査読国際誌

Soichiro Ibaragi, Norie Yoshioka, Hiroko Kishikawa, Jamie K Hu, Peter M Sadow, Ming Li, Guo-fu Hu

Molecular cancer research : MCR 7 ( 3 ) 415 - 24 2009年3月

記述言語：英語

Angiogenin (ANG), originally identified as an angiogenic ribonuclease, has recently been shown to play a direct role in prostate cancer cell proliferation by mediating rRNA transcription. ANG is up-regulated in human prostate cancer and is the most significantly up-regulated gene in AKT-driven prostate intraepithelial neoplasia (PIN) in mice. Enhanced cell proliferation in the PIN lesions requires increased ribosome biogenesis, a multistep process involving an orchestrated production of ribosomal proteins and rRNA. AKT is known to enhance ribosomal protein production through the mammalian target of rapamycin pathway. However, it was unknown how rRNA is proportionally increased. Here, we report that ANG is essential for AKT-driven PIN formation and survival. We showed that up-regulation of ANG in the AKT-overexpressing mouse prostates is an early and lasting event. It occurs before PIN initiation and lasts beyond PIN is fully developed. Knocking down ANG expression by intraprostate injection of lentivirus-mediated ANG-specific small interfering RNA prevents AKT-induced PIN formation without affecting AKT expression and its signaling through the mammalian target of rapamycin pathway. Neomycin, an aminoglycoside that blocks nuclear translocation of ANG, and N65828, a small-molecule enzymatic inhibitor of the ribonucleolytic activity of ANG, both prevent AKT-induced PIN formation and reverse established PIN. They also decrease nucleolar organizer region, restore cell size, and normalize luminal architectures of the prostate despite continuous activation of AKT. All three types of the ANG inhibitor suppress rRNA transcription of the prostate luminal epithelial cells and inhibit AKT-induced PIN, indicating an essential role of ANG in AKT-mediated cell proliferation and survival.

DOI： 10.1158/1541-7786.MCR-08-0137

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Epithelial-Mesenchymal Transition Induced by Growth Suppressor p12(CDK2-AP1) Promotes Tumor Cell Local Invasion but Suppresses Distant Colony Growth 査読国際誌

Takanori Tsuji, Soichiro Ibaragi, Kaori Shima, Miaofen G. Hu, Miki Katsurano, Akira Sasaki, Guo-fu Hui

CANCER RESEARCH 68 ( 24 ) 10377 - 10386 2008年12月

Nicotine promotes mammary tumor migration via a signaling cascade involving protein kinase C and CDC42. 査読国際誌

Jinjin Guo, Soichiro Ibaragi, Tongbo Zhu, Ling-Yu Luo, Guo-Fu Hu, Petra S Huppi, Chang Yan Chen

Cancer research 68 ( 20 ) 8473 - 81 2008年10月

記述言語：英語

Nicotine, one of the major components in tobacco, is at high concentrations in the bloodstream of cigarette smokers. However, the mechanisms of how nicotine affects tumor development and whether nicotine is a potential carcinogen for malignancies induced by secondhand smoking are not fully understood yet. Here, we investigate the signaling pathways by which nicotine potentiates tumorigenesis in human mammary epithelial-like MCF10A or cancerous MCF7 cells. We show that human MCF10A and MCF7 cells both express four subunits of nicotine acetylcholine receptor (nAChR). The treatment of these cells with nicotine enhances the activity of protein kinase C (PKC) alpha without altering the expression level of this kinase. Nicotine also stimulates [(3)H]thymidine incorporation into the genome of these cells as well as forces serum-starved cells to enter S phase of the cell cycle, resulting in growth promotion. Importantly, on nicotine treatment, the mobility of MCF10A and MCF7 cells is enhanced, which can be blocked by the addition of nAChR or PKC inhibitor. Experiments using small interfering RNA knockdown or ectopic expression of cdc42 showed that cdc42 functions as a downstream effector of PKC and is crucial in the regulation of nicotine-mediated migratory activity in the cells. Together, our findings suggest that nicotine, through interacting with its receptor, initiates a signaling cascade that involves PKC and cdc42 and consequently promotes migration in mammary epithelial or tumor cells.

DOI： 10.1158/0008-5472.CAN-08-0131

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Novel transcription-factor-like function of human matrix metalloproteinase 3 regulating the CTGF/CCN2 gene. 査読国際誌

Takanori Eguchi, Satoshi Kubota, Kazumi Kawata, Yoshiki Mukudai, Junji Uehara, Toshihiro Ohgawara, Soichiro Ibaragi, Akira Sasaki, Takuo Kuboki, Masaharu Takigawa

Molecular and cellular biology 28 ( 7 ) 2391 - 413 2008年4月

記述言語：英語

Matrix metalloproteinase 3 (MMP3) is well known as a secretory endopeptidase that degrades extracellular matrices. Recent reports indicated the presence of MMPs in the nucleus (A. J. Kwon et al., FASEB J. 18:690-692, 2004); however, its function has not been well investigated. Here, we report a novel function of human nuclear MMP3 as a trans regulator of connective tissue growth factor (CCN2/CTGF). Initially, we cloned MMP3 cDNA as a DNA-binding factor for the CCN2/CTGF gene. An interaction between MMP3 and transcription enhancer dominant in chondrocytes (TRENDIC) in the CCN2/CTGF promoter was confirmed by a gel shift assay and chromatin immunoprecipitation. The CCN2/CTGF promoter was activated by overexpressed MMP3, whereas a TRENDIC mutant promoter lost the response. Also, the knocking down of MMP3 suppressed CCN2/CTGF expression. By cytochemical and histochemical analyses, MMP3 was detected in the nuclei of chondrocytic cells in culture and also in the nuclei of normal and osteoarthritic chondrocytes in vivo. The nuclear translocation of externally added recombinant MMP3 and six putative nuclear localization signals in MMP3 also were shown. Furthermore, we determined that heterochromatin protein gamma coordinately regulates CCN2/CTGF by interacting with MMP3. The involvement of this novel role of MMP3 in the development, tissue remodeling, and pathology of arthritic diseases through CCN2/CTGF regulation thus is suggested.

DOI： 10.1128/MCB.01288-07

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SOX9 is expressed in human fetal prostate epithelium and enhances prostate cancer invasion 査読国際誌

Hongyun Wang, Irwin Leav, Soichiro Ibaragi, Michael Wegner, Guo-Fu Hu, Michael L. Lu, Steven P. Balk, Xin Yuan

CANCER RESEARCH 68 ( 6 ) 1625 - 1630 2008年3月

Possible Involvement of p38 MAP Kinase in Retinoidstimulated Expression of Indian Hedgehog in Prehypertrophic Chondrocytes 査読

Tsuyoshi Shimo, Eiki Koyama, Soichiro Ibaragi, Naito Kurio, Daisuke Yamamoto, Tatsuo Okui, Koji Kishimoto, Hiroshi Mese, Akira Sasaki

Oral Science International 5 ( 1 ) 1 - 14 2008年

Specific inhibitor of MEK-mediated cross-talk between ERK and p38 MAPK during differentiation of human osteosarcoma cells 査読国際誌

Tsuyoshi Shimo, Shinsuke Matsumura, Soichiro Ibaragi, Sachiko Isowa, Koji Kishimoto, Hiroshi Mese, Akiyoshi Nishiyama, Akira Sasaki

JOURNAL OF CELL COMMUNICATION AND SIGNALING 1 ( 2 ) 103 - 111 2007年9月

Docetaxelにより急性呼吸窮迫症候群(ARDS)が生じた口腔癌肺転移症例

目瀬浩, 吉濱泰斗, 中山周子, 伊原木聰一郎, 佐々木朗

癌と化学療法 34 ( 8 ) 1267 - 1269 2007年8月

Ornithine decarboxylase antizyme upregulates DNA-dependent protein kinase and enhances the nonhomologous end-joining repair of DNA double-strand breaks in human oral cancer cells 査読国際誌

Takanori Tsuji, Miki Katsurano, Soichiro Ibaragi, Kaori Shima, Akira Sasaki, Guo-fu Hu

BIOCHEMISTRY 46 ( 31 ) 8920 - 8932 2007年8月

末期口腔癌患者の褥瘡に対してチーム医療で取り組んだ1症例査読

梅原亜矢子, 中山周子, 塚本剛一, 矢尾真弓, 伊原木聰一郎, 岸本晃治, 目瀬浩, 佐々木朗

岡山歯学会雑誌 26 ( 1 ) 37 - 40 2007年6月

外科的治療とPaclitaxel,Cisplatin,5-FluorouracilによるAdjuvant Chemotherapyが奏効した下顎歯肉癌肺転移症例査読

塚本剛一, 伊原木聰一郎, 志茂剛, 大山和彦, 岸本晃治, 目瀬浩, 青江基, 木浦勝行, 佐々木朗

癌と化学療法 34 ( 4 ) 597 - 600 2007年4月

Pathogenic role of connective tissue growth factor (CTGF/CCN2) in osteolytic metastasis of breast cancer 査読国際誌

Tsuyoshi Shimo, Satoshi Kubota, Norie Yoshioka, Soichiro Ibaragi, Sachiko Isowa, Takanori Eguchi, Akira Sasaki, Masaharu Takigawa

JOURNAL OF BONE AND MINERAL RESEARCH 21 ( 7 ) 1045 - 1059 2006年7月

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