Researcher Database


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TANAKA Mamoru

FacultyGraduate School of Medical Sciences Department of Gastroenterology and Metabolism
PositionAssistant Professor
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Last Updated :2020/07/04

Researcher Profile and Settings

Education

  •  - 2011 03 , Nagoya City University
  •  - 2003 03 , Nagoya City University

Association Memberships

  • The Japanese Society of Gastroenterology
  • JAPAN GASTROENTEROLOGICAL ENDOSCOPY SOCIETY
  • JAPAN SOCIETY FOR LASER SURGERY AND MEDICINE
  • THE JAPANESE CANCER ASSOCIATION
  • JAPAN SOCIETY OF CLINICAL ONCOLOGY
  • THE JAPANESE SOCIETY OF INTERNAL MEDICINE

Research Activities

Research Areas

  • Life sciences, Gastroenterology

Published Papers

  • Proton-pump inhibitor-induced fundic gland polyps with hematemesis., Tanaka M, Kataoka H, Yagi T, Clinical journal of gastroenterology, 12, (2) 193 - 195, 04 , Refereed
  • New photodynamic therapy with next-generation photosensitizers., Kataoka H, Nishie H, Hayashi N, Tanaka M, Nomoto A, Yano S, Joh T, Annals of translational medicine, 5, (8) , 04 , Refereed
  • Neurofibroma of the esophagus complicating Von Recklinghausen's neurofibromatosis., Tanaka M, Kataoka H, Joh T, The American journal of gastroenterology, 108, (12) 1935 - 1936, 12 , Refereed
  • Diagnostic utility of small-caliber and conventional endoscopes for gastric cancer and analysis of endoscopic false-negative gastric cancers., Kataoka H, Mizuno K, Hayashi N, Tanaka M, Nishiwaki H, Ebi M, Mizoshita T, Mori Y, Kubota E, Tanida S, Kamiya T, Joh T, World journal of gastrointestinal endoscopy, 5, (9) 440 - 445, 09 , Refereed
  • TGF beta induces proHB-EGF shedding and EGFR transactivation through ADAM activation in gastric cancer cells, Masahide Ebi, Hiromi Kataoka, Takaya Shimura, Eiji Kubota, Yoshikazu Hirata, Takashi Mizushima, Tsutomu Mizoshita, Mamoru Tanaka, Motoshi Mabuchi, Hironobu Tsukamoto, Satoshi Tanida, Takeshi Kamiya, Shigeki Higashiyama, Takashi Joh, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 402, (3) 449 - 454, 11 , Refereed, Background and aims Transforming growth factor-beta (TGF beta) is known to potently inhibit cell growth Loss of responsiveness to TGB beta inhibition on cell growth is a hallmark of many types of cancer, yet its mechanism is not fully understood. Membrane-anchored heparin-binding EGF-like growth factor (proHB-EGF) ectodomain is cleaved by a disintegrin and metalloproteinase (ADAM) members and is implicated in epidermal growth factor receptor (EGFR) transactivation Recently, nuclear translocation of the C-terminal fragment (CTF) of pro-HB-EGF was found to induce cell growth We investigated the association between TGF beta and HB-EGF signal transduction via ADAM activation Materials and methods The CCK-8 assay in two gastric cancer cell lines was used to determine the effect for cell growth by TGF beta. The effect of two ADAM inhibitors was also evaluated Induction of EGFR phosphorylation by TGF beta was analyzed and the effect of the ADAM inhibitors was also examined Nuclear translocation of HB-EGF-CTF by shedding through ADAM activated by TGF beta was also analyzed EGFR transactivation, HB-EGF-CTF nuclear translocation, and cell growth were examined under the condition of ADAM17 knockdown Result. TGF beta-induced EGFR phosphorylation of which ADAM inhibitors were able to inhibit TGF beta induced shedding of proHB-EGF allowing HB-EGF-CTF to translocate to the nucleus ADAM inhibitors blocked this nuclear translocation TGF beta enhanced gastric cancer cell growth and ADAM inhibitors suppressed this effect. EGFR phosphorylation, HB-EGF-CTF nuclear translocation, and cell growth were suppressed in ADAM17 knockdown cells Conclusion HB-EGF-CTF nuclear translocation and EGFR transactivation from proHB-EGF shedding mediated by ADAM17 activated by TGF beta might be an important pathway of gastric cancer cell proliferation by TGF beta. (C) 2010 Elsevier Inc. All rights reserved

Misc

  • GIST(Gastrointestinal stromal tumor)に対する糖鎖連結クロリンを用いた新規光線力学的治療法(Photodynamic Therapy)の検討, 田中 守, 片岡 洋望, 赤司 治夫, 矢野 重信, 森田 明理, 城 卓志, 日本レーザー医学会誌, 32, (3) 338 - 338,   2011 10
  • 消化器癌に対するPDTの現状と将来展望 消化管癌PDTを目指した新しい光感受性物質の基礎検討, 片岡 洋望, 田中 守, 赤司 治夫, 矢野 重信, 森田 明理, 城 卓志, 日本レーザー医学会誌, 31, (3) 291 - 291,   2010 10
  • 糖鎖連結クロリンによる消化管癌に対する新規光線力学的治療法の開発 活性酸素の産生とアポトーシス誘導の検討, 田中 守, 片岡 洋望, 志村 貴也, 溝下 勤, 谷田 諭史, 神谷 武, 森田 明理, 矢野 重信, 城 卓志, G.I.Research, 18, (4) 374 - 375,   2010 08
  • 胃癌、大腸癌に対するグルコース結合クロリンによる新規光線力学的治療法(Novel photodynamic therapy with glucose conjugated chlorine for gastric and colon cancer), 田中 守, 片岡 洋望, 平田 慶和, 志村 貴也, 溝下 勤, 久保田 英嗣, 神谷 武, 森田 明理, 城 卓志, 日本癌学会総会記事, 69回,   2010 08
  • Blockage of angiotensin II type 1 receptor regulates TNF-alpha-induced MAdCAM-1 expression via inhibition of NF-kappa B translocation to the nucleus and ameliorates colitis, Takashi Mizushima, Makoto Sasaki, Tomoaki Ando, Tsuneya Wada, Mamoru Tanaka, Yasuyuki Okamoto, Masahide Ebi, Yosikazu Hirata, Kenji Murakami, Tsutomu Mizoshita, Takaya Shimura, Eiji Kubota, Naotaka Ogasawara, Satoshi Tanida, Hiromi Kataoka, Takeshi Kamiya, J. S. Alexander, Takashi Joh, AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 298, (2) G255 - G266,   2010 02 , Mizushima T, Sasaki M, Ando T, Wada T, Tanaka M, Okamoto Y, Ebi M, Hirata Y, Murakami K, Mizoshita T, Shimura T, Kubota E, Ogasawara N, Tanida S, Kataoka H, Kamiya T, Alexander JS, Joh T. Blockage of angiotensin II type 1 receptor regulates TNF-alpha-induced MAdCAM-1 expression via inhibition of NF-kappa B translocation to the nucleus and ameliorates colitis. Am J Physiol Gastrointest Liver Physiol 298: G255-G266, 2010. First published November 25, 2009; doi:10.1152/ajpgi.00264.2009.-Mucosal vascular addressin cell adhesion molecule 1 (MAdCAM-1) is an important target in the treatment of inflammatory bowel disease (IBD). Recently, treatment of IBD with an antibody to alpha 4 beta 7-integrin, a ligand for MAdCAM-1, has been an intense focus of research. Our aim was to clarify the mechanism by which MAdCAM-1 is regulated via angiotensin II type 1 receptor (AT1R), and to verify if AT1R might be a novel target for IBD treatment. The role of AT1R in the expression of MAdCAM-1 in SVEC (a murine high endothelial venule cell) and MJC-1 (a mouse colonic endothelial cell) was examined following cytokine stimulation. We further evaluated the effect of AT1R on the pathogenesis of immune-mediated colitis using AT1R-deficient (AT1R-/-) mice and a selective AT1R blocker. AT1R blocker significantly suppressed MAdCAM-1 expression induced by TNF-alpha, but did not inhibit phosphorylation of p38 MAPK or of I kappa B that modulate MAdCAM-1 expression. However, NF-kappa B translocation into the nucleus was inhibited by these treatments. In a murine colitis model induced by dextran sulfate sodium, the degree of colitis, judged by body weight loss, histological damage, and the disease activity index, was much milder in AT1R-/- than in wild-type mice. The expression of MAdCAM-1 was also significantly lower in AT1R-/- than in wild-type mice. These results suggest that AT1R regulates the expression of MAdCAM-1 under colonic inflammatory conditions through regulation of the translocation of NF-kappa B into the nucleus. Furthermore, inhibition of AT1R ameliorates colitis in a mouse colitis model. Therefore, AT1R might be one of new therapeutic target of IBD via regulation of MAdCAM-1.

Awards & Honors

  •   2013 , UEGWeek2013, Oral Free Paper Prize


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