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NIshioka Soichiro

Faculty of Medicine　Global Center for BiomedicalScience and EngineeringPostdoctoral Fellow

Researcher basic information

■ Degree
  • Biomedical Science and engineering, Graduate school of biomedical science and engineering, Mar. 2022
■ URL
researchmap URLホームページURL■ Various IDs
J-Global ID■ Educational Organization

Research activity information

■ Papers
  • 3D scanner's potential as a novel tool for lymphedema measurement in mouse hindlimb models.
    Dongkyung Seo; Riri Ito; Kosuke Ishikawa; Takahiro Miura; Yuhei Yamamoto; Yasuhito Onodera; Soichiro Nishioka; Yoichi M Ito; Kanako Fuyama; Taku Maeda
    Scientific reports, 15, 1, 3747, 3747, 30 Jan. 2025, [International Magazine]
    English, Scientific journal, Lymphedema is characterized by persistent swelling due to impaired lymphatic function and presents significant challenges in both research and clinical settings. Traditional contact-based measurement techniques such as paw thickness and circumferential measurements using calipers or silk thread are useful but limited by observer variability and measurement accuracy. Non-contact methods, including various imaging techniques, offer improvements but often at higher cost and complexity. In this study, we address the need for a more reliable, cost-effective, and non-invasive method for assessing lymphedema in mouse models. Here we show that 3D scanning technology can enhance the measurement of lymphedema in a mouse hindlimb model. Our results indicate that 3D scanners provide more consistent measurements with lower variability compared with conventional methods and without the need for direct contact, which could potentially alter the measurement outcomes. The findings of this study suggest that 3D scanning could replace traditional methods, offering a more standardized and less subjective tool for lymphedema research in the near future. This technology would not only improve upon conventional methods but also extend the capabilities for detailed anatomical analyses in small animal models, which could have implications for other areas of biomedical research.
  • The lipid-binding D4 domain of perfringolysin O facilitates the active loading of exogenous cargo into extracellular vesicles.
    Abayomi Emmanuel Opadele; Soichiro Nishioka; Ping-Hsiu Wu; Quynh-Thu Le; Hiroki Shirato; Jin-Min Nam; Yasuhito Onodera
    FEBS letters, 598, 4, 446, 456, Feb. 2024, [International Magazine]
    English, Scientific journal, Whereas extracellular vesicles (EVs) have been engineered for cargo loading, innovative strategies for it can still be developed. Here, we describe domain 4 (D4), a cholesterol-binding domain derived from perfringolysin O, as a viable candidate for EV cargo loading. D4 and its mutants localized to the plasma membrane and the membranes of different vesicular structures in the cytoplasm, and facilitate the transport of proteins of interest (POIs) into EVs. D4-EVs were internalized by recipient cells analogous to EVs engineered with CD9. Intracellular cargo discharge from D4-EVs was successfully detected with the assistance of vesicular stomatitis virus glycoprotein. This study presents a novel strategy for recruiting POIs into EVs via a lipid-binding domain that ensures content release in recipient cells.
  • Rab27b contributes to radioresistance and exerts a paracrine effect via epiregulin in glioblastoma.
    Soichiro Nishioka; Ping-Hsiu Wu; Toshiaki Yakabe; Amato J Giaccia; Quynh-Thu Le; Hidefumi Aoyama; Shinichi Shimizu; Hiroki Shirato; Yasuhito Onodera; Jin-Min Nam
    Neuro-oncology advances, 2, 1, vdaa091, 2020, [International Magazine]
    English, Scientific journal, BACKGROUND: Radiotherapy is the standard treatment for glioblastoma (GBM). However, radioresistance of GBM cells leads to recurrence and poor patient prognosis. Recent studies suggest that secretion factors have important roles in radioresistance of tumor cells. This study aims to determine whether Rab27b, a small GTPase involved in secretory vesicle trafficking, plays a role in radioresistance of GBM. METHODS: Microarray analysis, cell viability analysis, apoptosis assay, immunostaining, and in vivo experiments were performed to assess the effect of Rab27b on radioresistance of GBM. We further investigated paracrine effects mediated by Rab27b after X-ray irradiation using coculture systems of glioma cell lines. RESULTS: Rab27b was specifically upregulated in irradiated U87MG cells. Furthermore, Rab27b knockdown decreased the proliferation of GBM cells after irradiation. Knockdown of Rab27b in U87MG cells combined with radiation treatment suppressed orthotopic tumor growth in the mouse brain and prolonged the survival of recipient mice. Interestingly, the co-upregulation of Rab27b and epiregulin (EREG), a member of the epidermal growth factor (EGF) family, correlated with radioresistance in glioma cell lines. Additionally, EREG, which was secreted from U87MG cells via Rab27b-mediated mechanism, activated EGF receptor and contributed to H4 cell proliferation in a paracrine manner. CONCLUSIONS: Our results show that Rab27b mediates the radioresistance of highly malignant GBM cells. Rab27b promotes the proliferation of adjacent cells through EREG-mediated paracrine signaling after irradiation. Thus, the Rab27b-EREG pathway is a novel potential target to improve the efficacy of radiotherapy in GBM.
■ Other Activities and Achievements
■ Research Themes
  • Medical Mathematics for Fractionation Modulated Radiotherapy and its Treatment Planning
    Grants-in-Aid for Scientific Research
    01 Apr. 2024 - 31 Mar. 2029
    白土 博樹; 小野寺 康仁; 福永 久典; 水田 正弘; 加葉田 雄太朗; 深作 亮也; 西岡 蒼一郎; 小亀 翔揮
    Japan Society for the Promotion of Science, Grant-in-Aid for Scientific Research (C), Hokkaido University, 24K10903
  • Development of a new treatment for cancer cachexia - Verification of synergistic effects of inhibition of secreted factors and radiotherapy.
    Grants-in-Aid for Scientific Research
    01 Apr. 2024 - 31 Mar. 2027
    西岡 蒼一郎
    Japan Society for the Promotion of Science, Grant-in-Aid for Early-Career Scientists, Hokkaido University, 24K18750
  • Optimization of cancer treatment based on intra-tumor metabolic geometry
    Grants-in-Aid for Scientific Research
    07 Oct. 2021 - 31 Mar. 2026
    小野寺 康仁; 西岡 蒼一郎; Nam JinMin
    本年度は、腫瘍内の代謝微小環境を再現するin vitro解析系の改善と、それを用いたメカニズム解析に着手した。特に、栄養素濃度の不均一性によって生じる特殊な代謝微小環境において観察されるconventionalな治療法への耐性メカニズムの詳細について、分泌タンパク質に着目した解析を行った。また、今後のより詳細な解析において結果に無視できない影響を及ぼす懸念のある「栄養充足細胞からの微量グルコースの漏洩」について、その可能性を検討するための実験を行った。
    「栄養充足細胞」および「栄養欠乏細胞」の共存する条件（代謝協調状態）において特異的に分泌される何らかのタンパク質が両者の放射線耐性を高めると仮定し、両者の共培養系で得られる馴化培地に存在するタンパク質の解析を行った。細胞特異的な糖代謝制御に用いる「グルコース前駆体」を用いた「栄養充足細胞」（当該の前駆体をグルコースに転換して生存できる細胞）の単独培養や、通常グルコース濃度（5.5 mM）における「栄養充足細胞」および「栄養欠乏細胞」（ただしこの場合はいずれも栄養充足状態になる）の共培養などを比較対象として、馴化培地中のタンパク質（アルブミンを除く）を回収した。これらをアクリルアミドゲル電気泳動で分離して銀染色を行ったところ、代謝協調状態において特異的に認められる幾つかのタンパク質バンドが確認できた。現在、質量分析による当該タンパク質の同定を進めている。
    また、「栄養充足細胞」および「栄養欠乏細胞」の共培養条件における、前者からのグルコース漏出が後者の生存性維持に寄与し得るか検討するため、後者における解糖系代謝酵素GPIのノックダウンを行った。GPIノックダウン細胞の単独培養は増殖および生存を著しく阻害したが、共培養下では影響がほとんど見られなかったことから、僅かに漏出するグルコースの寄与は殆ど無視できるものと判断できた。
    Japan Society for the Promotion of Science, Fund for the Promotion of Joint International Research (Fostering Joint International Research (B)), Hokkaido University, 21KK0140