Updated on 2025/03/04

写真a

 
YAMAGISHI Ryota
 
Organization
Graduate School of Medicine Department of Basic Medical Science Lecturer
School of Medicine Department of Medical Science
Title
Lecturer
Affiliation
Institute of Medcine

Position

  • Graduate School of Medicine Department of Basic Medical Science 

    Lecturer  2023.10 - Now

  • Graduate School of Medicine Department of Basic Medical Science 

    Assistant Professor  2022.04 - 2023.09

  • School of Medicine Department of Medical Science 

    Lecturer  2023.10 - Now

  • School of Medicine Department of Medical Science 

    Assistant Professor  2022.04 - 2023.09

Degree

  • 博士（薬学） （ Nagoya City University ）

Research Areas

  • Life Science / Tumor biology

Research Interests

  • がん微小環境、細胞老化、mRNA代謝

Research subject summary

  • 転写後調節を介したがん微小環境制御

Professional Memberships

  • 日本癌学会

      Domestic

  • 日本がん分子標的学会

      Domestic

  • 日本肝臓学会

      Domestic

Awards

  • 日本癌学会奨励賞

    2023.09   日本癌学会  

  • 大阪公立大学医学部長賞(優秀賞)

    2023.03   大阪公立大学  

  • 大阪公立大学若手研究者奨励賞 南部陽一郎記念若手奨励賞

    2022.12   大阪公立大学  

  • The APASL Single Topic Conference 2021 in Osaka、Young Investigator Award

    2021.09  

Job Career (off-campus)

  • 大阪市立大学大学院医学研究科   病態生理学

    2017.10 - 2022.03

  • 愛知県がんセンター   分子腫瘍学部   リサーチレジデント

    2016.04 - 2017.09

Education

  • Nihon University     Graduated/Completed

  • Nagoya City University   The second semester of doctoral program   Graduated/Completed

Papers

  • Regular exercise suppresses steatosis-associated liver cancer development by degrading E2F1 and c-Myc via circadian gene upregulation. Reviewed

    Vu Thuong Huyen, Kanae Echizen, Ryota Yamagishi, Miho Kumagai, Yoshiki Nonaka, Takahiro Kodama, Tatsuya Ando, Megumu Yano, Naoki Takada, Masaki Takasugi, Fumitaka Kamachi, Naoko Ohtani

    Genes to cells : devoted to molecular & cellular mechanisms   29 ( 11 )   1012 - 1025   2024.11（ ISSN:1356-9597 ）

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    Authorship：Lead author   Publishing type：Research paper (scientific journal)   International / domestic magazine：International journal  

    Regular exercise is believed to suppress cancer progression. However, the precise molecular mechanisms by which exercise prevents cancer development remain unclear. In this study, using a steatosis-associated liver cancer mouse model, we found that regular exercise at a speed of 18 m/min for 20 min daily suppressed liver cancer development. To explore the underlying mechanisms, we examined the gene expression profiles in the livers of the exercise and non-exercise groups. The expressions of circadian genes, such as Per1 and Cry2, were upregulated in the exercise group. As circadian rhythm disruption is known to cause various diseases, including cancer, improving circadian rhythm through exercise could contribute to cancer prevention. We further found that the expression of a series of E2F1 and c-Myc target genes that directly affect the proliferation of cancer cells was downregulated in the exercise group. However, the expression of E2F1 and c-Myc was transcriptionally unchanged but degraded at the post-translational level by exercise. Cry2, which is regulated by the Skp1-Cul1-FBXL3 (SCFFBXL3) ubiquitin ligase complex by binding to FBXL3, can form a complex with E2F1 and c-Myc, which we think is the mechanism to degrade them. Our study revealed a previously unknown mechanism by which exercise prevents cancer development.

    DOI： 10.1111/gtc.13161

    PubMed

  • Concerted action of ataxin-2 and PABPC1-bound mRNA poly(A) tail in the formation of stress granules. Reviewed

    Ryota Yamagishi, Hiroto Inagaki, Jun Suzuki, Nao Hosoda, Haruka Sugiyama, Kazunori Tomita, Takashi Hotta, Shin-Ichi Hoshino

    Nucleic acids research   2024.06

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    Authorship：Lead author   Publishing type：Research paper (scientific journal)   International / domestic magazine：International journal  

    Stress induces global stabilization of the mRNA poly(A) tail (PAT) and the assembly of untranslated poly(A)-tailed mRNA into mRNPs that accumulate in stress granules (SGs). While the mechanism behind stress-induced global PAT stabilization has recently emerged, the biological significance of PAT stabilization under stress remains elusive. Here, we demonstrate that stress-induced PAT stabilization is a prerequisite for SG formation. Perturbations in PAT length impact SG formation; PAT shortening, achieved by overexpressing mRNA deadenylases, inhibits SG formation, whereas PAT lengthening, achieved by overexpressing their dominant negative mutants or downregulating deadenylases, promotes it. PABPC1, which specifically binds to the PAT, is crucial for SG formation. Complementation analyses reveal that the PABC/MLLE domain of PABPC1, responsible for binding PAM2 motif-containing proteins, plays a key role. Among them, ataxin-2 is a known SG component. A dominant-negative approach reveals that the PAM2 motif of ataxin-2 is essential for SG formation. Notably, ataxin-2 increases stress sensitivity, lowering the threshold for SG formation, probably by promoting the aggregation of PABPC1-bound mRNA. The C-terminal region is responsible for the self-aggregation of ataxin-2. These findings underscore the critical roles of mRNA PAT, PABPC1 and ataxin-2 in SG formation and provide mechanistic insights into this process.

    DOI： 10.1093/nar/gkae497

    PubMed

  • 増大特集 代謝 Ⅲ.代謝とがん 腸内細菌叢成分の肝移行による肥満関連肝がんの進展機構 Reviewed

    山岸 良多, 大谷 直子

    生体の科学   74 ( 5 )   460 - 461   2023.10（ ISSN:03709531 ） （ eISSN:18835503 ）

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    Publishing type：Research paper (scientific journal)  

    DOI： 10.11477/mf.2425201753

  • SMG6 regulates DNA damage and cell survival in Hippo pathway kinase LATS2-inactivated malignant mesothelioma. Reviewed

    Suzuki K, Tange M, Yamagishi R, Hanada H, Mukai S, Sato T, Tanaka T, Akashi T, Kadomatsu K, Maeda T, Miida T, Takeuchi I, Murakami H, Sekido Y, Murakami-Tonami Y

    Cell death discovery   8 ( 1 )   446   2022.11（ ISSN:2058-7716 ）

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    Publishing type：Research paper (scientific journal)  

    DOI： 10.1038/s41420-022-01232-w

    PubMed

  • mTOR- and LARP1-dependent regulation of TOP mRNA poly(A) tail and ribosome loading. Reviewed

    Koichi Ogami, Yuka Oishi, Kentaro Sakamoto, Mayu Okumura, Ryota Yamagishi, Takumi Inoue, Masaya Hibino, Takuto Nogimori, Natsumi Yamaguchi, Kazuya Furutachi, Nao Hosoda, Hiroto Inagaki, Shin-Ichi Hoshino

    Cell reports   41 ( 4 )   111548 - 111548   2022.10

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    Publishing type：Research paper (scientific journal)   International / domestic magazine：International journal  

    Translation of 5' terminal oligopyrimidine (TOP) mRNAs encoding the protein synthesis machinery is strictly regulated by an amino-acid-sensing mTOR pathway. However, its regulatory mechanism remains elusive. Here, we demonstrate that TOP mRNA translation positively correlates with its poly(A) tail length under mTOR active/amino-acid-rich conditions, suggesting that TOP mRNAs are post-transcriptionally controlled by poly(A) tail-length regulation. Consistent with this, the tail length of TOP mRNAs dynamically fluctuates in response to amino acid availability. The poly(A) tail shortens under mTOR active/amino-acid-rich conditions, whereas the long-tailed TOP mRNAs accumulate under mTOR inactive/amino-acid-starved (AAS) conditions. An RNA-binding protein, LARP1, is indispensable for the process. LARP1 interacts with non-canonical poly(A) polymerases and induces post-transcriptional polyadenylation of the target. Our findings illustrate that LARP1 contributes to the selective accumulation of TOP mRNAs with long poly(A) tails under AAS, resulting in accelerated ribosomal loading onto TOP mRNAs for the resumption of translation after AAS.

    DOI： 10.1016/j.celrep.2022.111548

    PubMed

  • Cancer cells produce liver metastasis via gap formation in sinusoidal endothelial cells through proinflammatory paracrine mechanisms. Reviewed

    Huu Hoang T, Sato-Matsubara M, Yuasa H, Matsubara T, Thuy LTT, Ikenaga H, Phuong DM, Hanh NV, Hieu VN, Hoang DV, Hai H, Okina Y, Enomoto M, Tamori A, Daikoku A, Urushima H, Ikeda K, Dat NQ, Yasui Y, Shinkawa H, Kubo S, Yamagishi R, Ohtani N, Yoshizato K, Gracia-Sancho J, Kawada N

    Science advances   8 ( 39 )   eabo5525   2022.09

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    Publishing type：Research paper (scientific journal)  

    DOI： 10.1126/sciadv.abo5525

    PubMed

  • Gasdermin D-mediated release of IL-33 from senescent hepatic stellate cells promotes obesity-associated hepatocellular carcinoma. Reviewed

    Yamagishi R, Kamachi F, Nakamura M, Yamazaki S, Kamiya T, Takasugi M, Cheng Y, Nonaka Y, Yukawa-Muto Y, Thuy LTT, Harada Y, Arai T, Loo TM, Yoshimoto S, Ando T, Nakajima M, Taguchi H, Ishikawa T, Akiba H, Miyake S, Kubo M, Iwakura Y, Fukuda S, Chen WY, Kawada N, Rudensky A, Nakae S, Hara E, Ohtani N

    Science immunology   7 ( 72 )   eabl7209   2022.06

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    Publishing type：Research paper (scientific journal)  

    DOI： 10.1126/sciimmunol.abl7209

    PubMed

  • Non-heat-stressed Method to Isolate Hepatic Stellate Cells From Highly Steatotic Tumor-bearing Liver Using CD49a. Reviewed

    Cheng Y, Yamagishi R, Nonaka Y, Sato-Matsubara M, Kawada N, Ohtani N

    Cellular and molecular gastroenterology and hepatology   14 ( 4 )   964 - 966.e9   2022

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    Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.jcmgh.2022.07.006

    PubMed

  • Gut microbial metabolite and obesity-associated liver cancer Reviewed

    Ohtani Naoko, Kamiya Tomonori, Kamachi Fumitaka, Yamagishi Ryota

    CANCER SCIENCE   112   1031 - 1031   2021.02（ ISSN:1347-9032 ）

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    Publishing type：Research paper (scientific journal)  

  • The mechanism of SASP in obesity-associated liver tumor microenvironnment Reviewed

    Yamagishi Ryota, Kamachi Fumitaka, Cheng Yi, Hara Eiji, Ohtani Naoko

    CANCER SCIENCE   112   488 - 488   2021.02（ ISSN:1347-9032 ）

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    Publishing type：Research paper (scientific journal)  

  • Molecular mechanism of synthetic lethality induced by SMG6 inhibition in LATS2-mutated mesothelioma cells Reviewed

    Suzuki Koya, Yamagishi Ryota, Mukai Satomi, Tabe Yoko, Miida Takashi, Sekido Yoshitaka, Murakami-Tonami Yuko

    CANCER SCIENCE   112   628 - 628   2021.02（ ISSN:1347-9032 ）

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    Publishing type：Research paper (scientific journal)  

  • The RNA-binding protein QKI-7 recruits the poly(A) polymerase GLD-2 for 3' adenylation and selective stabilization of microRNA-122. Reviewed

    Hojo H, Yashiro Y, Noda Y, Ogami K, Yamagishi R, Okada S, Hoshino SI, Suzuki T

    The Journal of biological chemistry   295 ( 2 )   390 - 402   2020.01（ ISSN:0021-9258 ）

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    Publishing type：Research paper (scientific journal)  

    DOI： 10.1074/jbc.RA119.011617

    PubMed

  • SGO1 is involved in the DNA damage response in MYCN-amplified neuroblastoma cells. Reviewed

    Murakami-Tonami Y, Ikeda H, Yamagishi R, Inayoshi M, Inagaki S, Kishida S, Komata Y, Jan Koster, Takeuchi I, Kondo Y, Maeda T, Sekido Y, Murakami H, Kadomatsu K

    Scientific reports   6   31615   2016.08

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    Publishing type：Research paper (scientific journal)  

    DOI： 10.1038/srep31615

    PubMed

  • The STAR protein QKI-7 recruits PAPD4 to regulate post-transcriptional polyadenylation of target mRNAs. Reviewed

    Yamagishi R, Tsusaka T, Mitsunaga H, Maehata T, Hoshino S

    Nucleic acids research   44 ( 6 )   2475 - 90   2016.04（ ISSN:0305-1048 ）

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    Publishing type：Research paper (scientific journal)  

    DOI： 10.1093/nar/gkw118

    PubMed

  • Arsenite inhibits mRNA deadenylation through proteolytic degradation of Tob and Pan3. Reviewed

    Yamagishi R, Hosoda N, Hoshino S

    Biochemical and biophysical research communications   455 ( 3-4 )   323 - 31   2014.12（ ISSN:0006-291X ）

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    Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.bbrc.2014.11.015

    PubMed

  • Anti-proliferative protein Tob negatively regulates CPEB3 target by recruiting Caf1 deadenylase. Reviewed

    Hosoda N, Funakoshi Y, Hirasawa M, Yamagishi R, Asano Y, Miyagawa R, Ogami K, Tsujimoto M, Hoshino S

    The EMBO journal   30 ( 7 )   1311 - 23   2011.04（ ISSN:0261-4189 ）

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    Publishing type：Research paper (scientific journal)  

    DOI： 10.1038/emboj.2011.37

    PubMed

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MISC

  • 【MAFLD/MASHと免疫関係因子の進捗1】老化肝星細胞におけるガスダーミンD活性化とSASP因子放出 Reviewed

    山岸 良多, 大谷 直子

    臨床免疫・アレルギー科   81 ( 5 )   439 - 444   2024.05（ ISSN:1881-1930 ）

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

  • Activation of gasdermin D and SASP factor release from senescenset hepatic stellate cells. Reviewed

    山岸良多, 大谷直子

    月刊臨床免疫・アレルギー科   81 ( 5 )   2024（ ISSN:1881-1930 ）

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

    J-GLOBAL

  • 【代謝】代謝とがん　腸内細菌叢成分の肝移行による肥満関連肝がんの進展機構 Reviewed

    山岸 良多, 大谷 直子

    生体の科学   74 ( 5 )   460 - 461   2023.10（ ISSN:0370-9531 ）

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

    ＜文献概要＞腸内細菌叢は様々な代謝物質を産生し,それらが腸から吸収され,腸のみならず様々な遠隔臓器に影響を及ぼすことが明らかになっている。なかでも肝臓は,門脈などを介して腸内細菌関連因子がまず流れ込む臓器であり,腸内細菌叢の影響を受けやすい臓器と考えられる。筆者らは非アルコール性脂肪性肝炎関連肝がんの微小環境において,腸内細菌叢成分の肝移行により,肝がん促進的がん微小環境が形成されていることを見いだした。特に肝星細胞ががん関連線維芽細胞に変化し,細胞老化随伴分泌現象を起こす分子メカニズムの一端を明らかにした。

Presentations

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Industrial Property Rights

  • 固形がんの予防及び/又は治療薬

    大谷 直子, 山岸 良多

    　More details

    property_type：Patent 

    Application no：特願2023-016848 

    Announcement no：特開2023-116414 

    J-GLOBAL

Grant-in-Aid for Scientific Research

  • パイロトーシス実行因子GSDMDを標的としたCAF化肝星細胞排除法の開発

    Grant-in-Aid for Scientific Research(C)  2025

  • パイロトーシス実行因子GSDMDを標的としたCAF化肝星細胞排除法の開発

    Grant-in-Aid for Scientific Research(C)  2024

  • パイロトーシス実行因子GSDMDを標的としたCAF化肝星細胞排除法の開発

    Grant-in-Aid for Scientific Research(C)  2023

  • mRNA分解制御に着目した肥満誘導性肝がん新規治療標的の探索

    Grant-in-Aid for Early-Career Scientists  2022

  • 合成致死を利用した悪性中皮腫瘍新規治療標的の探索

    Grant-in-Aid for Young Scientists(B)  2017.04

Contract research

  • 肝微小血管構成細胞由来セクリトームとその関連遺伝子のバイオインフォマティックス解析に基づく肝硬変の分子理解と治療法開発

    国立研究開発法人日本医療研究開発機構  保健衛生医療調査等推進事業費補助金／肝炎等克服実用化研究事業  2024

  • 運動による肝がん抑制分子メカニズムの解明：運動効果を模倣する治療法の開発

    国立研究開発法人日本医療研究開発機構  保健衛生医療調査等推進事業費補助金／肝炎等克服実用化研究事業  2024

  • 運動による肝がん抑制分子メカニズムの解明：運動効果を模倣する治療法の開発

    国立研究開発法人 日本医療研究開発機構  肝炎等克服実用化研究事業  2023

  • 肝微小血管構成細胞由来セクリトームとその関連遺伝子のバイオインフォマティックス解析に基づく肝硬変の分子理解と治療法開発

    国立研究開発法人日本医療研究開発機構  保健衛生医療調査等推進事業費補助金／肝炎等克服実用化研究事業  2023

  • 肝微小血管構成細胞由来セクリトームとその関連遺伝子のバイオインフォマティックス解析に基づく肝硬変の分子理解と治療法開発

    国立研究開発法人日本医療研究開発機構  保健衛生医療調査等推進事業費補助金／肝炎等克服実用化研究事業  2022

Charge of on-campus class subject

  • 初年次ゼミナール

    2024   Weekly class   Undergraduate

  • 医学研究推進コース3

    2024   Practical Training   Undergraduate

  • 機能系実習

    2024   Practical Training   Undergraduate

  • 内分泌・代謝

    2024     Undergraduate

  • 医学研究推進コース3

    2023   Practical Training   Undergraduate

  • 機能系実習

    2023   Practical Training   Undergraduate

  • 内分泌・代謝

    2023     Undergraduate

  • 医学研究推進コース3

    2022   Practical Training   Undergraduate

  • 機能系実習

    2022   Practical Training   Undergraduate

  • 内分泌・代謝

    2022     Undergraduate

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Number of papers published by graduate students

  • 2024

    Number of graduate students presentations：1

Number of instructed thesis, researches

  • 2024

    Number of instructed the graduation thesis：1  Number of graduation thesis reviews：1

    [Number of instructed the Master's Program] (previous term)：1  [Number of instructed the Master's Program] (letter term)：3

  • 2023

    [Number of instructed the Master's Program] (letter term)：3

  • 2022

    [Number of instructed the Master's Program] (letter term)：2