研究者詳細 - 木下　理恵

MISC - 木下　理恵

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リンパ内皮細胞上のNOX4は癌細胞のリンパ系への遊走に重要な役割を果たす

山内明, 山村真弘, 片瀬直樹, 友信奈保子, 木下理恵, 阪口政清, 岡本秀一郎

日本癌学会学術総会抄録集(Web) 79th 2020年

細胞外S100A11によりがん間質線維芽細胞が加速する膵がん進展のメカニズムの解明

合原勇馬, 光井洋介, 友信奈保子, 木下理恵, 山内明, 山村真弘, 近藤英作, 豊岡伸一, 豊岡伸一, 那須保友, 阪口政清

日本癌学会学術総会抄録集(Web) 79th 2020年

分泌性S100A11は膵臓癌の細胞運動性を高める腫瘍周囲の線維芽細胞を活性化する

合原勇馬, 光井洋介, 友信奈保子, 木下理恵, 山本健一, 山内明, 山村真弘, 近藤英作, 豊岡伸一, 那須保友, 村田等, 阪口政清

日本分子生物学会年会プログラム・要旨集(Web) 43rd 2020年

キシリトールによるがん細胞選択的抗がん作用の分子機構の解明ならびにキシリトールの生体における抗がん効能の検討

友信奈保子, 合原勇馬, 木下理恵, 阪口政清

日本癌学会学術総会抄録集(Web) 79th 2020年

転移がんに有効なS100A8/A9阻害薬の開発(Novel therapeutic approach based on S100A8/A9-mediated organ tropic cancer metastasis)

木下理恵, 友信奈保子, 山内明, 枝園和彦, 冨田秀太, 村田等, 二見淳一郎, 近藤英作, 豊岡伸一, 阪口政清

日本癌学会総会記事 78回 P - 2252 2019年9月

MUSCAT-Assay法での自己抗体モニタリングによる腫瘍免疫応答評価

二見淳一郎, 本莊知子, 吉岡実咲, 勝河祐希, Ahmadi Hannaneh, 尾崎龍之介, 木下理恵, 鵜殿平一郎, 垣見和宏

日本がん免疫学会総会プログラム・抄録集 23回 141 - 141 2019年7月

メラノーマ原発巣における転移機構に関わるMCAM-S100A8/A9シグナル経路の分子学的解析

友信奈保子, 木下理恵, 近藤英作, 山内明, 二見淳一郎, 豊岡伸一, 阪口政清

日本癌学会学術総会抄録集(Web) 78th 2019年

膵がん進展に導く膵がん細胞間質線維芽細胞クロストークを介在する分泌性S100A11 受容体RAGE連携の役割

光井洋介, 山本健一, Sumardika I Wayan, 木下理恵, 村田等, 二見淳一郎, 高松仁, 山本靖彦, 西堀正洋, 豊岡伸一, 渡部昌実, 那須保友, 阪口政清

日本がん免疫学会総会プログラム・抄録集 22回 156 - 156 2018年7月

分泌性S100A11-受容体RAGEシグナルに着眼した膵がん間質増大のメカニズムの解明

山本健一, 高松仁, 光井洋介, 木下理恵, 村田等, 二見淳一郎, 山本靖彦, 西堀正洋, 豊岡伸一, 阪口政清

日本がん免疫学会総会プログラム・抄録集 22回 117 - 117 2018年7月

抗がん抗原抗体で腫瘍免疫応答をモニタリングするMUSCAT-Assay

二見淳一郎, 本莊知子, 吉岡実咲, 勝河祐希, Hannaneh Ahmadi, 木下理恵, 藤枝奈緒, 垣見和宏

日本がん免疫学会総会プログラム・抄録集 22回 122 - 122 2018年7月

分泌性S100A11-受容体RAGEシグナルに着眼した膵がん間質増大のメカニズムの解明

山本健一, 高松仁, 光井洋介, 木下理恵, 村田等, 二見淳一郎, 山本靖彦, 西堀正洋, 豊岡伸一, 阪口政清

日本がん免疫学会総会プログラム・抄録集 22回 117 - 117 2018年7月

膵がん進展に導く膵がん細胞間質線維芽細胞クロストークを介在する分泌性S100A11 受容体RAGE連携の役割

光井洋介, 山本健一, Sumardika I Wayan, 木下理恵, 村田等, 二見淳一郎, 高松仁, 山本靖彦, 西堀正洋, 豊岡伸一, 渡部昌実, 那須保友, 阪口政清

日本がん免疫学会総会プログラム・抄録集 22回 156 - 156 2018年7月

Signal Diversity of Receptor for Advanced Glycation End Products. 査読

Masakiyo Sakaguchi, Rie Kinoshita, Endy Widya Putranto, I Made Winarsa Ruma, I Wayan Sumardika, Chen Youyi, Naoko Tomonobu, Ken-Ichi Yamamoto, Hitoshi Murata

Acta medica Okayama 71 ( 6 ) 459 - 465 2017年12月

記述言語：英語出版者・発行元：OKAYAMA UNIV MED SCHOOL

The receptor for advanced glycation end products (RAGE) is involved in inflammatory pathogenesis. It functions as a receptor to multiple ligands such as AGEs, HMGB1 and S100 proteins, activating multiple intracellular signaling pathways with each ligand binding. The molecular events by which ligand-activated RAGE controls diverse signaling are not well understood, but some progress was made recently. Accumulating evidence revealed that RAGE has multiple binding partners within the cytoplasm and on the plasma membrane. It was first pointed out in 2008 that RAGE's cytoplasmic tail is able to recruit Diaphanous-1 (Dia-1), resulting in the acquisition of increased cellular motility through Rac1/Cdc42 activation. We also observed that within the cytosol, RAGE's cytoplasmic tail behaves similarly to a Toll-like receptor (TLR4)-TIR domain, interacting with TIRAP and MyD88 adaptor molecules that in turn activate multiple downstream signals. Subsequent studies demonstrated the presence of an alternative adaptor molecule, DAP10, on the plasma membrane. The coupling of RAGE with DAP10 is critical for enhancing the RAGE-mediated survival signal. Interestingly, RAGE interaction on the membrane was not restricted to DAP10 alone. The chemotactic G-protein-coupled receptors (GPCRs) formyl peptide receptors1 and 2 (FPR1 and FPR2) also interacted with RAGE on the plasma membrane. Binding interaction between leukotriene B4 receptor 1 (BLT1) and RAGE was also demonstrated. All of the interactions affected the RAGE signal polarity. These findings indicate that functional interactions between RAGE and various molecules within the cytoplasmic area or on the membrane area coordinately regulate multiple ligand-mediated RAGE responses, leading to typical cellular phenotypes in several pathological settings. Here we review RAGE's signaling diversity, to contribute to the understanding of the elaborate functions of RAGE in physiological and pathological contexts.

DOI： 10.18926/AMO/55582

Web of Science

PubMed

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Exogenous DKK-3/REIC inhibits Wnt/β-catenin signaling and cell proliferation in human kidney cancer KPK1 査読国際誌

Jiaqi Xu, Takuya Sadahira, Rie Kinoshita, Shun Ai Li, Peng Huang, Koichiro Wada, Motoo Araki, Kazuhiko Ochiai, Hirofumi Noguchi, Masakiyo Sakaguchi, Yasutomo Nasu, Masami Watanabe

Oncology Letters 14 ( 5 ) 5638 - 5642 2017年11月

Robust cancer-specific gene expression by a novel cassette with hTERT and CMV promoter elements 査読

Masakiyo Sakaguchi, Takuya Sadahira, Hideo Ueki, Rie Kinoshita, Hitoshi Murata, Ken-Ichi Yamamoto, Junichiro Futami, Yasutomo Nasu, Kazuhiko Ochiai, Hiromi Kumon, Nam-Ho Huh, Masami Watanabe

ONCOLOGY REPORTS 38 ( 2 ) 1108 - 1114 2017年8月

記述言語：英語出版者・発行元：SPANDIDOS PUBL LTD

We developed and validated a novel hTERT/CMV promoter element-driven gene expression cassette that can robustly enhance cancer-specific gene expression. The following gene expressional elements were located in tandem within the plasmid construct: [hTERT core promoter, cytomegalovirus (CMV) minimized promoter, RU5' sequence, an inserted gene, BGH polyA, hTERT enhancer]; this is hereafter referred to as the hT/Cm-R-hT construct. Using various human cancer cell lines and normal cells, the cancer-specific transcription of the green fluorescent protein (GFP) gene was examined by western blotting and fluorescence microscopy. Cancer-specific gene expression was robustly achieved in the hT/Cm-R-hT plasmid in comparison to the other control hT/Cm-driven construct. Notably, the expression level of GFP observed in the hT/Cm-RhT-driven construct was superior to that of the control plasmid with the conventional CMV promoter in HEK293 cells, which are known to possess higher hTERT activity than normal cells. We next examined the availability of hT/Cm-R-hT in detecting the target GFP expressing cancer cells from human peripheral blood mononuclear cells (PBMCs). The hT/Cm-R-hT plasmid successfully induced cancer-specific gene expression; the robust expression of GFP was observed in target HeLa cancer cells, whereas GFP was not visibly expressed in normal PBMCs. The plasmid allowed for the selective visualization of viable HeLa cancer cells in mixed cell cultures containing up to 10000-fold more PBMCs. These findings indicate that the hT/Cm-R-hT expressional system is a valuable tool for detecting viable cancer cells mixed with normal cells. The current system can therefore be applied to the in vitro detection of cancer cells that are disseminated in the blood and other types of body fluid in vivo. Since the current system can also be applied to other types of vectors, including virus vectors, this approach using the hTERT promoter-based construct is expected to become a valuable tool for enhancing cancer specific gene expression.

DOI： 10.3892/or.2017.5710

Web of Science

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Expression of tumor suppressor REIC/Dkk-3 by a newly improved adenovirus vector with insertion of a hTERT promoter at the 3'-side of the transgene 査読

Endy Widya Putranto, Rie Kinoshita, Masami Watanabe, Takuya Sadahira, Hitoshi Murata, Ken-Ichi Yamamoto, Junichiro Futami, Ken Kataoka, Yusuke Inoue, I. Made Winarsa Ruma, I. Wayan Sumardika, Chen Youyi, Miyoko Kubo, Yoshihiko Sakaguchi, Kenji Saito, Yasutomo Nasu, Hiromi Kumon, Nam-Ho Huh, Masakiyo Sakaguchi

ONCOLOGY LETTERS 14 ( 1 ) 1041 - 1048 2017年7月

記述言語：英語出版者・発行元：SPANDIDOS PUBL LTD

Reduced expression in immortalized cells (REIC)/Dickkopf-3 (Dkk-3) overexpression, induced using an adenovirus (Ad)-REIC, has been revealed to have a dramatic therapeutic effect on multiple types of cancer. To achieve an improved therapeutic effect from Ad-REIC on cancer, our group previously developed an enhanced gene expression system, the C-TSC cassette [cytomegalovirus (CMV)-RU5' located upstream (C); another promoter unit composed of triple tandem promoters, human telomerase reverse transcriptase (hTERT), simian virus 40 and CMV, located downstream of the cDNA (TSC); plus a polyadenylation (polyA) signal]. When applied to the conventional Ad-REIC, this novel system induced the development of an enhanced product, Ad-C-TSC-REIC, which exhibited a noticeable anticancer effect. However, there were difficulties in terms of Ad-C-TSC-REIC productivity in HEK293 cells, which are a widely used donor cell line for viral production. Productivity of Ad-C-TSC-REIC was significantly reduced compared with the conventional Ad-REIC, as the Ad-C-TSC-REIC had a significantly higher ability to induce apoptotic cell death of not only various types of cancer cell, but also HEK293 cells. The present study aimed to overcome this problem by modifying the C-TSC structure, resulting in an improved candidate: A C-T cassette (C: CMV-RU5' located upstream; T: another promoter unit composed of a single hTERT promoter, located downstream of the cDNA plus a polyA signal), which demonstrated gene expression comparable to that of the C-TSC system. The improved adenovirus REIC/Dkk-3 product with the C-T cassette, named Ad-C-T-REIC, exhibited a higher expression level of REIC/Dkk3, similar to that of Ad-C-TSC-REIC. Notably, the vector mitigated the cell death of donor HEK293 cells, resulting in a higher rate of production of its adenovirus. These results indicated that Ad-C-T-REIC has the potential to be a useful tool for application in cancer gene therapy.

DOI： 10.3892/ol.2017.6201

Web of Science

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Topics from special edition 転移先臓器を感知する受容体群の分子制御機構の解明とその応用

阪口政清, 木下理恵, 村田等, 山本健一, 許南浩, 日比野利彦

細胞 49 ( 7 ) 359 - 362 2017年6月

Topics from special edition 転移先臓器を感知する受容体群

阪口政清, 木下理恵, 村田等, 山本健一, 許南浩, 日比野利彦

細胞 49 ( 3 ) 143 - 146 2017年3月

ß-1,3-galactosyl-O-glycosyl-glycoprotein ß-1,6-N-acetylglucosaminyltransferase 3 Increases MCAM Stability, Which Enhances S100A8/A9-Mediated Cancer Motility. 査読

Sumardika IW, Youyi C, Kondo E, Inoue Y, Ruma IMW, Murata H, Kinoshita R, Yamamoto KI, Tomida S, Shien K, Satoh H, Yamauchi A, Futami J, Putranto EW, Hibino T, Toyooka S, Nishibori M, Sakaguchi M

Oncol Res 2017年

Neuroplastinβとextracellular matrix metalloprotease inducerはS100A8/A9に対する機能的な受容体であり，ケラチノサイトの増殖とアトピーの皮膚炎症の増強に関与している. Critical role of novel receptors to S100A8/A9, EMMPRIN and NPTNβ, on keratinocyte growth and inflammation in atopic dermatitis.

阪口政清, 山本真実, 宮井雅史, 松元有羽子, 木下理恵, 村田等, 山本健一, 森実真, 岩月啓氏, 許南浩, 坪井良治, 日比野利彦

臨床免疫 49 ( 6 ) 594 - 598 2017年

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