写真a

KAWAUCHI Keiko

Position

Associate Professor

Research Field

Life Science / Molecular biology, Life Science / Tumor biology

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Graduating School 【 display / non-display

  • Himeji Institute of Technology   Faculty of Science   Graduated

    1991.4 - 1995.3

Graduate School 【 display / non-display

  • 姫路工業大学大学院   理学研究科   生命科学専攻   Doctor's Course   Completed

    1998.4 - 2002.3

Campus Career 【 display / non-display

  • KONAN UNIVERSITY   Faculty of Frontiers of Innovative Research in Science and Technology   Faculty of Frontiers of Innovative Research in Science and Technology Department of Nanobiochemistry   Associate Professor

    2018.4

  • KONAN UNIVERSITY   Faculty of Frontiers of Innovative Research in Science and Technology   Faculty of Frontiers of Innovative Research in Science and Technology Department of Nanobiochemistry   Lecturer

    2014.4 - 2018.3

External Career 【 display / non-display

  • 神戸大学大学院   工学研究科

    2021.12

  • 日本医科大学   先端医学研究所

    2014.4 - 2021.3

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    Country:Japan

  • National University of Singapore   Mechanobiology Institute

    2010.5 - 2014.3

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    Country:Singapore

  • 日本医科大学   老人病研究所

    2008.10 - 2011.12

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    Country:Japan

  • 日本医科大学   老人病研究所

    2007.4 - 2008.9

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    Country:Japan

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Papers 【 display / non-display

  • Loss of p53 function promotes DNA damage-induced formation of nuclear actin filaments. Reviewed International journal

    Takeru Torii, Wataru Sugimoto, Katsuhiko Itoh, Natsuki Kinoshita, Masaya Gessho, Toshiyuki Goto, Ikuno Uehara, Wataru Nakajima, Yemima Budirahardja, Daisuke Miyoshi, Takahito Nishikata, Nobuyuki Tanaka, Hiroaki Hirata, Keiko Kawauchi

    Cell death & disease   14 ( 11 )   766 - 766   2023.11

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    Joint Work

    Authorship:Last author, Corresponding author  

    Tumor suppressor p53 plays a central role in response to DNA damage. DNA-damaging agents modulate nuclear actin dynamics, influencing cell behaviors; however, whether p53 affects the formation of nuclear actin filaments remains unclear. In this study, we found that p53 depletion promoted the formation of nuclear actin filaments in response to DNA-damaging agents, such as doxorubicin (DOXO) and etoposide (VP16). Even though the genetic probes used for the detection of nuclear actin filaments exerted a promotive effect on actin polymerization, the detected formation of nuclear actin filaments was highly dependent on both p53 depletion and DNA damage. Whilst active p53 is known to promote caspase-1 expression, the overexpression of caspase-1 reduced DNA damage-induced formation of nuclear actin filaments in p53-depleted cells. In contrast, co-treatment with DOXO and the pan-caspase inhibitor Q-VD-OPh or the caspase-1 inhibitor Z-YVAD-FMK induced the formation of nuclear actin filament formation even in cells bearing wild-type p53. These results suggest that the p53-caspase-1 axis suppresses DNA damage-induced formation of nuclear actin filaments. In addition, we found that the expression of nLifeact-GFP, the filamentous-actin-binding peptide Lifeact fused with the nuclear localization signal (NLS) and GFP, modulated the structure of nuclear actin filaments to be phalloidin-stainable in p53-depleted cells treated with the DNA-damaging agent, altering the chromatin structure and reducing the transcriptional activity. The level of phosphorylated H2AX (γH2AX), a marker of DNA damage, in these cells also reduced upon nLifeact-GFP expression, whilst details of the functional relationship between the formation of nLifeact-GFP-decorated nuclear actin filaments and DNA repair remained to be elucidated. Considering that the loss of p53 is associated with cancer progression, the results of this study raise a possibility that the artificial reinforcement of nuclear actin filaments by nLifeact-GFP may enhance the cytotoxic effect of DNA-damaging agents in aggressive cancer cells through a reduction in gene transcription.

    DOI: 10.1038/s41419-023-06310-0

    PubMed

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  • Development of a pseudo-cellular system to quantify specific interactions determining G-quadruplex function in cells. Reviewed International journal

    Journal of the American Chemical Society   146 ( 12 )   8005 - 8015   2024.2

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    Publisher:Journal of the American Chemical Society  

  • Inhibitory Effects of Shikonin Dispersion, an Extract of Lithospermum erythrorhizon Encapsulated in β-1,3-1,6 Glucan, on Streptococcus mutans and Non-Mutans Streptococci. Reviewed International journal

    Ryota Nomura, Yuto Suehiro, Fumikazu Tojo, Saaya Matayoshi, Rena Okawa, Masakazu Hamada, Shuhei Naka, Michiyo Matsumoto-Nakano, Rika Unesaki, Kazuya Koumoto, Keiko Kawauchi, Takahito Nishikata, Tatsuya Akitomo, Chieko Mitsuhata, Masatoshi Yagi, Toshiro Mizoguchi, Koki Fujikawa, Taizo Taniguchi, Kazuhiko Nakano

    International journal of molecular sciences   25 ( 2 )   2024.1

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    Shikonin is extracted from the roots of Lithospermum erythrorhizon, and shikonin extracts have been shown to have inhibitory effects on several bacteria. However, shikonin extracts are difficult to formulate because of their poor water solubility. In the present study, we prepared a shikonin dispersion, which was solubilized by the inclusion of β-1,3-1,6 glucan, and analysed the inhibitory effects of this dispersion on Streptococcus mutans and non-mutans streptococci. The shikonin dispersion showed pronounced anti-S. mutans activity, and inhibited growth of and biofilm formation by this bacterium. The shikonin dispersion also showed antimicrobial and antiproliferative effects against non-mutans streptococci. In addition, a clinical trial was conducted in which 20 subjects were asked to brush their teeth for 1 week using either shikonin dispersion-containing or non-containing toothpaste, respectively. The shikonin-containing toothpaste decreased the number of S. mutans in the oral cavity, while no such effect was observed after the use of the shikonin-free toothpaste. These results suggest that shikonin dispersion has an inhibitory effect on S. mutans and non-mutans streptococci, and toothpaste containing shikonin dispersion may be effective in preventing dental caries.

    DOI: 10.3390/ijms25021075

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  • Inhibitory Effect of Adsorption of Streptococcus mutans onto Scallop-Derived Hydroxyapatite. Reviewed International journal

    Momoko Usuda, Mariko Kametani, Masakazu Hamada, Yuto Suehiro, Saaya Matayoshi, Rena Okawa, Shuhei Naka, Michiyo Matsumoto-Nakano, Tatsuya Akitomo, Chieko Mitsuhata, Kazuya Koumoto, Keiko Kawauchi, Takahito Nishikata, Masatoshi Yagi, Toshiro Mizoguchi, Koki Fujikawa, Taizo Taniguchi, Kazuhiko Nakano, Ryota Nomura

    International journal of molecular sciences   24 ( 14 )   2023.7

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    Hydroxyapatite adsorbs various substances, but little is known about the effects on oral bacteria of adsorption onto hydroxyapatite derived from scallop shells. In the present study, we analyzed the effects of adsorption of Streptococcus mutans onto scallop-derived hydroxyapatite. When scallop-derived hydroxyapatite was mixed with S. mutans, a high proportion of the bacterial cells adsorbed onto the hydroxyapatite in a time-dependent manner. An RNA sequencing analysis of S. mutans adsorbed onto hydroxyapatite showed that the upregulation of genes resulted in abnormalities in pathways involved in glycogen and histidine metabolism and biosynthesis compared with cells in the absence of hydroxyapatite. S. mutans adsorbed onto hydroxyapatite was not killed, but the growth of the bacteria was inhibited. Electron microscopy showed morphological changes in S. mutans cells adsorbed onto hydroxyapatite. Our results suggest that hydroxyapatite derived from scallop shells showed a high adsorption ability for S. mutans. This hydroxyapatite also caused changes in gene expression related to the metabolic and biosynthetic processes, including the glycogen and histidine of S. mutans, which may result in a morphological change in the surface layer and the inhibition of the growth of the bacteria.

    DOI: 10.3390/ijms241411371

    PubMed

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  • The iron chelator deferriferrichrysin induces paraptosis via extracellular-signal-regulated kinase activation in cancer cells Reviewed International coauthorship

    Kinoshita N, Gessho M, Torii T, Ashida Y, Akamatsu M, Guo AK, Lee S, Katsuno T, Nakajima W, Budirahardja Y, Miyoshi D, Todokoro T, Ishida H, Nishikata T, Kawauchi K

    Genes to Cells   28 ( 9 )   653 - 662   2023.6

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    Authorship:Last author, Corresponding author  

    DOI: doi.org/10.1111/gtc.13053

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Books and Other Publications 【 display / non-display

  • 相分離生物学の全貌

    三好大輔, 川内敬子(DNA・RNAと相分離)

    現代化学増刊  2020.11 

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  • がん研究読本 6

    川内敬子(RASによるがん悪性化に、p53を介したアクチン細胞骨格の変化がブレーキをかける道筋を解明!)

    がん研究分野の特性等を踏まえた支援活動総括支援活動班  2016 

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  • ゼロからはじめるバイオ実験マスター3細胞培養トレーニング

    西方敬人, 川上純司, 藤井敏司, 長濱宏治, 川内敬子( Role: Joint author)

    学研メディカル集潤社  2015.3 

  • 細胞培養トレーニング

    西方 敬人, 川上 純司, 藤井 敏司, 長濱 宏治, 川内 敬子

    学研メディカル秀潤社, 学研マーケティング (発売)  2015  ( ISBN:9784780909036

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Review Papers (Misc) 【 display / non-display

  • RNA高次構造を標的とした光線力学的療法の展望 Invited

    BIO Clinica   38 ( 13 )   76 - 78   2023.11

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    Publishing type:Article, review, commentary, editorial, etc. (scientific journal)  

  • 細胞内環境で安定化される核酸非構造を狙った分子標的薬の開発 Invited

    川内敬子・橋本佳樹・杉本 渉・三好大輔

    バイオマテリアル-生体材料   40 ( 3 )   206 - 211   2022.8

  • “Development of New Materials and New Functions for Biomaterials” Molecularly Targeted Molecules for Non-Canonical Nucleic Acid Structures Stabilized Under Cellular Molecular Crowding Conditions

    川内敬子, 橋本佳樹, 杉本渉, 三好大輔

    バイオマテリアル(Web)   40 ( 3 )   2022

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  • Future perspective of ligands for G-quadruplex nucleic acids as therapeutic agents

    木下菜月, 取井猛流, 川内敬子, 三好大輔

    Bio Clinica   37 ( 4 )   2022

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  • Photodynamic therapy targeting nucleic acid G-quadruplexes

    取井猛流, 木下菜月, 浦野諒人, 三好大輔, 川内敬子

    日本女性科学者の会学術誌(Web)   22   2022

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Presentations 【 display / non-display

  • グアニン四重らせん構造により制御される長鎖非コードRNA Invited

    川内敬子、三好大輔

    第46回日本分子生物学会  (兵庫)  2023.12 

  • Emerging roles of actin in p53-dependent DNA damage responses Invited

    Keiko Kawauchi

    The 10th International MDM2 workshop  2023.10 

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    Country:Japan  

  • がん細胞における核酸のグアニン四重らせん構造の機能の解明とその制御法の確立

    川内敬子、建石寿枝、杉本直己、三好大輔

    2022年度先端モデル動物支援プラットフォーム 成果発表会  2023.2 

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    Event date: 2023.2

  • 液-液相分子により形成されるグアニン四重らせん構造集合体の役割 Invited

    川内敬子、取井猛流、谷口慎也、木下菜月、建石寿枝、杉本直己、三好大輔

    第45回日本分子生物学会  2022.12 

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    Event date: 2022.11 - 2022.12

  • Structural alterations in ribosomal DNA under nucleolar stress Invited

    Keiko Kawauchi, Takeru Torii, Hisae Karimata Tateishi, Naoki Sugimoto, Takahito Nishikata, Daisuke Miyoshi

    The 44th Annual Meeting of Molecular Biology Society of Japan  2021.12 

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    Event date: 2021.12

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Industrial property rights 【 display / non-display

  • 核酸の立体構造を制御する方法及びその用途、並びに、細胞内分子クラウディング環境を再現するための組成物

    建石 寿枝、川内 敬子、高橋 俊太郎、杉本 直己

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    Application no:特願2022-189538

  • 光増感剤輸送キャリア

    大谷 亨、川内 敬子、三好 大輔

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    Application no:特願2022-128296

Academic Awards Received 【 display / non-display

  • 日本女性科学者の会奨励賞

    2021.5   日本女性科学者の会  

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  • 村尾育英会 学術賞

    2019.3   一般財団法人 村尾育英会  

    川内敬子

  • 神奈川難病財団研究奨励賞

    2008.12   神奈川難病財団  

    川内敬子

Grant-in-Aid for Scientific Research 【 display / non-display

  • 「匂いシグナル」で制御される口腔がん細胞の細胞融合誘導機構の解析

    2022.4 - 2025.3

    JSPS Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research(C)

    荒木 啓吾, 川内 敬子

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  • Model system for nucleic acid-protein liquid-liquid phase separation

    2021.4 - 2024.3

    JSPS Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research(B)

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  • がん抑制因子p53の機能低下が惹起する異常な核小体ストレス応答の分子機構解明

    2021.4 - 2024.3

    JSPS Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research(C)

    川内 敬子

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  • Formation and function of nucleolus depending on rRNA G-quadruplexes

    2020.7 - 2022.3

    JSPS Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Research (Exploratory)

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  • Regulation of stress granule formation by RNA G-quadruplex

    2018.6 - 2020.3

    JSPS Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Research (Exploratory)

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Other External funds procured 【 display / non-display

  • DNA高次構造によるレトロトランスポゾンLINE-1遺伝子の転写調節機構の解明とその制御法の探索

    2024.1 - 2025.3

    公益財団法人第一三共生命科学研究振興財団  研究助成金 

  • 低酸素ストレス耐性を獲得したがん細胞を標的とした治療薬の開発

    2023.1 - 2024.3

    公益財団法人テルモ生命科学振興財団  研究開発助成金  財団等研究助成金

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    Authorship:principal_investigator 

  • 核内アクチン線維構造の制御による 新たながん治療創薬への挑戦

    2018.4 - 2020.3

    甲南学園  甲南学園平生太郎基金科学研究奨励助成金

 

Committee Memberships 【 display / non-display

  • 2021.6   日本学術会議 総合工学委員会科学的知見の創出に資する可視化分科会  細胞-身体可塑基盤からの自分を知り育てる科学的知見創出に資する可視化小委員会委員

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  • 2021.6 - 2023.9   日本学術会議 総合工学委員会科学的知見の創出に資する可視化分科会  細胞-身体可塑基盤からの自分を知り育てる科学的知見創出に資する可視化小委員会委員

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  • 2021.5   日本女性科学者の会  日本女性科学者の会 理事

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Social Activities 【 display / non-display

  • 新型コロナウイルス感染症のPCR検査の原理を知る

    Role(s): Lecturer

    御影高等学校  2021.11

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  • がん細胞の謎を解く~がんの予防と治療に向けて~

    Role(s): Lecturer

    JR東日本  東京オトナ大学  2019.12

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  • 『がん』とは?

    Role(s): Lecturer

    東京海上日動火災保険(株)・甲南大学  公開講座  2017.11

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  • ダイバーシティ研究環境整備と女性研究者の未来

    Role(s): Panelist

    日経グループ  日経ウーマノミクスプロジェクト  2017.5

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