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 141 - 160 件目／全件表示 >>

伊原木聰一郎, 西山明慶, 奥井達雄, 栗尾奈愛, 柴田茜, 岸本晃治, 志茂剛, 佐々木朗

日本口腔診断学会雑誌 27 ( 1 ) 27 - 31 2014年2月

A Case of Fibrous Dysplasia of the Mandible with Histopathological Evaluation after Long-term Observation

SOICHIRO IBARAGI, AKIYOSHI NISHIYAMA, TATSUO OKUI, NAITO KURIO, AKANE SHIBATA, KOJI KISHIMOTO, TSUYOSHI SHIMO, AKIRA SASAKI

Japanese Journal of Oral Diagnosis / Oral Medicine 27 ( 1 ) 27 - 31 2014年

Angiogenin mediates androgen-stimulated prostate cancer growth and enables castration resistance. 査読国際誌

Shuping Li, Miaofen G Hu, Yeqing Sun, Norie Yoshioka, Soichiro Ibaragi, Jinghao Sheng, Guangjie Sun, Koji Kishimoto, Guo-Fu Hu

Molecular cancer research : MCR 11 ( 10 ) 1203 - 14 2013年10月

記述言語：英語掲載種別：研究論文（学術雑誌）

UNLABELLED: The androgen receptor (AR) is a critical effector of prostate cancer development and progression. Androgen-dependent prostate cancer is reliant on the function of AR for growth and progression. Most castration-resistant prostate cancer (CRPC) remains dependent on AR signaling for survival and growth. Ribosomal RNA (rRNA) is essential for both androgen-dependent and castration-resistant growth of prostate cancer cells. During androgen-dependent growth of prostate cells, androgen-AR signaling leads to the accumulation of rRNA. However, the mechanism by which AR regulates rRNA transcription is unknown. Here, investigation revealed that angiogenin (ANG), a member of the secreted ribonuclease superfamily, is upregulated in prostate cancer and mediates androgen-stimulated rRNA transcription in prostate cancer cells. Upon androgen stimulation, ANG undergoes nuclear translocation in androgen-dependent prostate cancer cells, where it binds to the rDNA promoter and stimulates rRNA transcription. ANG antagonists inhibit androgen-induced rRNA transcription and cell proliferation in androgen-dependent prostate cancer cells. Interestingly, ANG also mediates androgen-independent rRNA transcription through a mechanism that involves its constitutive nuclear translocation in androgen-insensitive prostate cancer cells, resulting in a constant rRNA overproduction and thereby stimulating cell proliferation. Critically, ANG overexpression in androgen-dependent prostate cancer cells enables castration-resistant growth of otherwise androgen-dependent cells. Thus, ANG-stimulated rRNA transcription is not only an essential component for androgen-dependent growth of prostate cancer but also contributes to the transition of prostate cancer from androgen-dependent to castration-resistant growth status. IMPLICATIONS: The ability of angiogenin to regulate rRNA transcription and prostate cancer growth makes it a viable target for therapy.

DOI： 10.1158/1541-7786.MCR-13-0072

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エナメル上皮腫摘出後に骨移植と骨延長により骨増量を行ったインプラント治療の1例

伊原木聰一郎, 目瀬浩, 中山周子, 兒玉真一, 奥井達雄, 吉岡徳枝, 岸本晃治, 中妻可奈子, 志茂剛, 佐々木朗

Japanese Journal of Maxillo Facial Implants 12 ( 2 ) 53 - 57 2013年8月

咽頭弁により経鼻挿管困難であった唇顎口蓋裂患者に対し経口挿管で上下顎同時移動術を行った1例

西山明慶, 吉岡徳枝, 伊原木聰一郎, 國定勇希, 福島宏明, 村上隆, 山城隆, 佐々木朗

日本顎変形症学会雑誌 23 ( 2 ) 108 - 108 2013年5月

Novel HSP90 inhibitor NVP-AUY922 enhances the anti-tumor effect of temsirolimus against oral squamous cell carcinoma. 査読国際誌

Tatsuo Okui, Tsuyoshi Shimo, Takuya Fukazawa, Nur Mohammad Monsur Hassan, Tatsuki Honami, Soichiro Ibaragi, Munenori Takaoka, Yoshio Naomoto, Akira Sasaki

Current cancer drug targets 13 ( 3 ) 289 - 99 2013年3月

記述言語：英語掲載種別：研究論文（学術雑誌）

BACKGROUND AND AIM: Heat shock protein 90 (HSP90) and mammalian target of rapamycin (mTOR) are involved in the molecular pathogenesis of advanced oral squamous cell carcinoma. HSP90 inhibitors are capable of effectively interfering with multiple signaling pathways, including the mTOR signaling pathway. However, the combined effects of HSP90 and mTOR inhibitors on oral squamous cell carcinoma are still unknown. In this study, we investigated the dual treatment of the novel HSP90 inhibitor NVP-AUY922 and temsirolimus against oral squamous cell carcinoma. MATERIALS AND METHODS: The effect of the combination of NVP-AUY922 and temsirolimus on oral squamous cell carcinoma in vitro and in vivo was determined by MTS assay and mouse xenograft models. The effect of the combination on angiogenesis was determined by tube formation assay and angioreactor. RESULTS: The combination treatment of NVP-AUY922 and temsirolimus significantly inhibited the proliferation of SAS oral squamous cell carcinoma cells in vitro and suppressed the growth of oral squamous cell carcinoma xenografts in vivo. We have clearly shown that the combination treatment of NVP-AUY922 and temsirolimus inhibited vascular formation both in vitro and in vivo. Moreover, the combination treatment of NVP-AUY922 and temsirolimus prolonged the survival rate in mice xenografted with oral squamous cell carcinoma. CONCLUSIONS: Here, we showed the activity of a combination of mTOR and HSP90 inhibitors for the treatment of advanced oral squamous carcinoma.

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リンパ管新生の分子機構とリンパ浮腫

伊原木聰一郎

上原記念生命科学財団研究報告集 26 1 - 6 2012年12月

Hypoxia-induced up-regulation of angiogenin, besides VEGF, is related to progression of oral cancer. 査読国際誌

Koji Kishimoto, Shoko Yoshida, Soichiro Ibaragi, Norie Yoshioka, Tatsuo Okui, Guo-fu Hu, Akira Sasaki

Oral oncology 48 ( 11 ) 1120 - 7 2012年11月

記述言語：英語掲載種別：研究論文（学術雑誌）

OBJECTIVES: Angiogenin (ANG) is a prominent angiogenic factor that has been shown to have a dual effect on tumor progression by inducing both angiogenesis and cancer cell proliferation through stimulating ribosomal RNA transcription in both endothelial cells and cancer cells. In the present study, we investigated the expression profiles of ANG and vascular endothelial growth factor (VEGF) in oral cancer and their correlation with hypoxia and evaluated the possible value of ANG as a therapeutic target for oral cancer. MATERIALS AND METHODS: Immunohistochemistry (IHC), ELISA, real-time RT-PCR and Western blotting were used to examine the expression of ANG, VEGF, and hypoxia-inducible factor 1α (HIF-1α) in oral squamous cell carcinoma (OSCC) specimens and human OSCC cell lines. In order to examine the role of ANG, we knocked down ANG expression in HSC-2 cells by means of plasmid-mediated RNA interference. RESULTS: IHC showed that the expression of ANG was significantly correlated with that of HIF-1α in 50 OSCC specimens (P = 0.031). However, no significant correlation between VEGF and HIF-1α expression was found (P = 0.243). Consistently, ANG secretion increased under hypoxia in all of the 10 OSCC cell lines tested; and a significant increase was observed in 6 of them. In contrast, there was no noticeable increase in VEGF secretion under hypoxia in any of these cell lines. In HSC-2 and SAS OSCC cells, the increase in ANG mRNA expression correlated very well with that of HIF-1α protein expression after hypoxia onset. However, no noticeable increase in VEGF mRNA expression was observed even after 12 h of hypoxia. Down-regulation of ANG expression in HSC-2 cells highly expressing and secreting VEGF inhibited ribosome biogenesis, cell proliferation, tumor angiogenesis, and xenograft growth in athymic mice. CONCLUSION: These results suggest that ANG is up-regulated in the hypoxic environment of oral cancers and that its inhibition can have a therapeutic implication.

DOI： 10.1016/j.oraloncology.2012.05.009

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幼児の上顎歯肉に発生した巣状口腔粘液症の1例

伊原木聰一郎, 西山明慶, 吉岡徳枝, 片瀬直樹, 長塚仁, 佐々木朗

日本口腔外科学会雑誌 58 ( 9 ) 546 - 549 2012年9月

後期高齢者口腔扁平上皮癌症例の臨床的検討

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

日本口腔腫瘍学会誌 24 ( 3 ) 103 - 111 2012年9月

二つの拡大装置と外科的急速拡大の組み合わせによって治療を行った顔面非対称症例

川邉紀章, 古森紘基, 白賀のり子, 伊原木聰一郎, 吉岡徳枝, 西山明慶, 佐々木朗, 山城隆

日本矯正歯科学会大会プログラム・抄録集 71回 263 - 263 2012年9月

下顎骨腫瘍摘出後の骨折および顔貌変形防止に対するプレートの応用

岸本晃治, 吉田祥子, 銅前昇平, 帆波辰基, 伊原木聰一郎, 奥井達雄, 栗尾奈愛, 中妻可奈子, 佐々木朗

岡山歯学会雑誌 31 ( 1 ) 15 - 19 2012年6月

二つの拡大装置を用いた外科的急速拡大によって上顎歯列弓幅径の改善を行った顔面非対称症例

川邉紀章, 古森紘基, 伊原木聰一郎, 吉岡徳枝, 西山明慶, 佐々木朗, 山城隆

日本顎変形症学会雑誌 22 ( 2 ) 177 - 177 2012年5月

診断力てすと口腔粘膜のびらん

伊原木聰一郎, 佐々木朗

DENTAL DIAMOND 37 ( 1 ) 143 - 144 2012年1月

幼児の上顎歯肉粘液腫の1例

伊原木聰一郎, 西山明慶, 吉岡徳枝, 兒玉真一, 長塚仁, 目瀬浩, 佐々木朗

日本口腔科学会雑誌 61 ( 1 ) 182 - 182 2012年1月

Angiogenin as a molecular target for the treatment of prostate cancer. 査読国際誌

Shuping Li, Soichiro Ibaragi, Guo-Fu Hu

Current cancer therapy reviews 7 ( 2 ) 83 - 90 2011年5月

記述言語：英語

Angiogenin (ANG), a 14 kDa angiogenic ribonuclease, is upregulated in human prostate cancers, especially in hormone refractory diseases, and is the highest upregulated gene in Akt-driven prostate intraepithelial neoplasia (PIN) in mice. ANG has been shown to undergo nuclear translocation in both prostate cancer cells and cancer-associated endothelial cells where it binds to the promoter region of ribosomal DNA (rDNA) and stimulates ribosomal RNA (rRNA) transcription. ANG thus plays an essential role in prostate cancer progression by stimulating both cancer cell proliferation and tumor angiogenesis. A variety of ANG antagonists, including its antisense oligonucleotide, siRNA, soluble binding proteins, monoclonal antibody, enzymatic inhibitors, and nuclear translocation blockers, have all been shown to inhibit prostate cancer in various animal models. Accumulating evidence indicates that ANG is a molecular target for prostate cancer drug development.

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Induction of MMP-13 expression in bone-metastasizing cancer cells by type I collagen through integrin α1β1 and α2β1-p38 MAPK signaling. 査読国際誌

Soichiro Ibaragi, Tsuyoshi Shimo, Nur Mohammad Monsur Hassan, Sachiko Isowa, Naito Kurio, Hiroki Mandai, Shinichi Kodama, Akira Sasaki

Anticancer research 31 ( 4 ) 1307 - 13 2011年4月

記述言語：英語

BACKGROUND: Breast cancer cells frequently metastasize to the skeleton and produce and secrete proteinases, such as matrix metalloproteinase-13 (MMP-13), which promote destruction of the bone matrix. However, the mechanism of MMP-13 expression induced in areas of bone metastasis is unknown. Here, the interaction between tumors and type I collagen in bone metastasis was investigated. MATERIALS AND METHODS: A mouse model of bone metastasis was prepared by inoculating mice with suspensions of cells of the human metastatic breast cancer cell line MDA-MB-231 via the left cardiac ventricle. MMP-13 expression was examined by immunohistochemical, Western blot, and real-time RT-PCR analyses. RESULTS: MMP-13 expression was highly up-regulated in MDA-MB-231 cells, and attachment of these cells to type I collagen and the induction of MMP-13 were down-regulated by treatment with integrin α1, α2 or β1 neutralizing antibodies. The attachment of MDA-MB-231 cells to type I collagen induced the activation of focal adhesion kinase (FAK) and p38 mitogen-activated protein kinase (MAPK). Inhibition of FAK and p38 MAPK down-regulated type I collagen-induced MMP-13 expression. CONCLUSION: Our study indicates that metastatic breast cancer cells in the bone microenvironment attached to type I collagen, which stimulated integrins α1β1 and α2β1, via FAK and p38 MAPK pathways, to induce MMP13 expression and further osteolysis.

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Parathyroid hormone-related peptide regulates matrix metalloproteinase-13 gene expression in bone metastatic breast cancer cells. 査読国際誌

Soichiro Ibaragi, Tsuyoshi Shimo, Masahiro Iwamoto, Nur Mohammad Monsur Hassan, Shinichi Kodama, Sachiko Isowa, Akira Sasaki

Anticancer research 30 ( 12 ) 5029 - 36 2010年12月

記述言語：英語

BACKGROUND: Breast cancer (BC) cells often metastasize to bone where they express large amounts of parathyroid hormone-related protein (PTHrP). In this study, we investigated the possibility that PTHrP may have roles in breast cancer bone metastasis independently of, or in addition to, its roles in osteoclastic function. MATERIALS AND METHODS: A mouse model of bone metastasis was prepared by inoculating mice with suspensions of the human BC cell line MDA-MB-231 tumor cells via the left cardiac ventricle. Matrix metalloproteinase-13 (MMP-13) expression in the bone microenvironment was examined by Western blot and Real-time RT-PCR (RT-PCR) analysis, as well as by confocal microscopy. RESULTS: The invading MDA-MB-231 cells contained conspicuous amounts of both PTHrP and MMP-13, an important matrix-degrading enzyme; and treatment of the cells in culture with exogenous PTHrP markedly stimulated MMP13 gene expression. Analysis of signaling mechanisms showed that PTHrP treatment led to rapid increases in the levels of phosphorylated protein kinase C (PKCα) and extracellular signal-regulated kinase (ERK1/2). Pharmacologic inhibition of ERK1/2 and PKC as well as of PKA activities counteracted the PTHrP-dependent stimulation of MMP13 expression. Indeed, pharmacologic activation of PKA or PKC was sufficient for stimulation of MMP13 expression. CONCLUSION: Consistent with these findings, the inhibition of PKC prevented PTHrP-induced activation of ERK1/2, whereas 12-O-tetradecanoylphorbol-13-acetate (TPA), a stimulator of PKC, up-regulated the PTHrP-induced activation of ERK1/2. Taken together, our data indicate that the MDA-MB-231 breast cancer cells may carry out bone destruction and favor their own metastatic behavior by producing MMP-13. Given that the cells expressed PTHrP and that this factor stimulated MMP-13 expression, metastatic bone destruction may result from a PTHrP autocrine loop involving a PKC-ERK1/2 signaling pathway.

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口腔癌切除後の創部に対してポリグリコール酸フェルトとフィブリン糊を併用した被覆法の使用経験

伊原木聰一郎, 岸本晃治, 吉岡徳枝, 銅前昇平, 志茂剛, 中妻可奈子, 辻本紗代子, 栗尾奈愛, 兒玉真一, 武部祐一郎, 堀切優, 柴田茜, 西山明慶, 目瀬浩, 佐々木朗

岡山歯学会雑誌 29 ( 2 ) 107 - 112 2010年12月

PTHrP regulates angiogenesis and bone resorption via VEGF expression. 査読国際誌

Sachiko Isowa, Tsuyoshi Shimo, Soichiro Ibaragi, Naito Kurio, Tatsuo Okui, Kiminori Matsubara, Nur Mohammad Monsur Hassan, Koji Kishimoto, Akira Sasaki

Anticancer research 30 ( 7 ) 2755 - 67 2010年7月

記述言語：英語

BACKGROUND: Parathyroid hormone-related protein (PTHrP) is a key regulator of osteolytic metastasis of breast cancer (BC) cells, but its targets and mechanisms of action are not fully understood. This study investigated whether/how PTHrP (1-34) signaling regulates expression of vascular endothelial growth factor (VEGF) produced by BC cells. MATERIALS AND METHODS: A mouse model of bone metastasis was prepared by inoculating mice with tumour cell suspensions of the human BC cell line MDA-MB-231 via the left cardiac ventricle. VEGF expression was examined by Western blot and real-time RT-PCR analysis, as well as by confocal microscopy in the bone microenvironment. RESULTS: PTHrP was expressed in cancer cells producing PTH/PTHrP receptor and VEGF that had invaded the bone marrow, and PTHrP was up-regulated VEGF in MDA-MB-231 in vitro. The culture medium conditioned by PTHrP-treated MDA-MB-231 cells stimulated angiogenesis and osteoclastogenesis compared with control medium, giving a response that was inhibited by VEGF-neutralizing antibody treatment. Inhibition of protein kinase C (PKC) prevented PTHrP-induced extracellular signal-regulated kinase (ERK1/2) and p38 activation, and PTHrP-induced VEGF expression. CONCLUSION: PTHrP plays an important role in modulating the angiogenic and bone osteolytic actions of VEGF through PKC-dependent activation of an ERK1/2 and p38 signaling pathway during bone metastasis by breast cancer cells.

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