Details of the Researcher

PHOTO

Atsuko Kasahara
Section
Graduate School of Life Sciences
Job title
Assistant Professor
Degree

  • the Degree of Doctor of Philosophy in Science (University of Tsukuba)

Research History 3

  • 2016 - 2024
    金沢大学 がん進展制御研究所

  • 2008 - 2014
    University of Geneva

  • 2015 -
    University of Padua

Education 3

  • 筑波大学 大学院 生命環境科学研究科 情報生物科学専攻 (博士課程）

    2004 - 2006

  • University of Tsukuba

    2002 - 2004

  • 筑波大学 第二学群 生物学類

    1998 - 2002

Professional Memberships 2

  • 日本生化学会

  • 日本ミトコンドリア学会

Research Areas 1

  • Life sciences / Cell biology /

Papers 18

  1. Lysine-arginine imbalance overcomes therapeutic tolerance governed by the transcription factor E3-lysosome axis in glioblastoma. International-journal

    Yongwei Jing, Masahiko Kobayashi, Mahmoud I Shoulkamy, Meiqi Zhou, Ha Thi Vu, Hiroshi Arakawa, Hemragul Sabit, Sadahiro Iwabuchi, Cong Quang Vu, Atsuko Kasahara, Masaya Ueno, Yuko Tadokoro, Kenta Kurayoshi, Xi Chen, Yuhang Yan, Satoshi Arai, Shinichi Hashimoto, Tomoyoshi Soga, Tomoki Todo, Mitsutoshi Nakada, Atsushi Hirao

    Nature communications　16　(1)　2876-2876　2025/04/01

    DOI： 10.1038/s41467-025-56946-z 　

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    Recent advances in cancer therapy have underscored the importance of targeting specific metabolic pathways. In this study, we propose a precision nutrition approach aimed at lysosomal function in glioblastoma multiforme (GBM). Using patient-derived GBM cells, we identify lysosomal activity as a unique metabolic biomarker of tumorigenesis, controlling the efficacy of temozolomide (TMZ), a standard GBM therapy. Employing combined analyses of clinical patient samples and xenograft models, we further elucidate the pivotal role of Transcription Factor Binding To IGHM Enhancer 3 (TFE3), a master regulator of lysosomal biogenesis, in modulating malignant properties, particularly TMZ tolerance, by regulating peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC1α)-mediated mitochondrial activity. Notably, we find that lysine protects GBM cells from lysosomal stress by counteracting arginine's effects on nitric oxide production. The lysine restriction mimetic, homoarginine administration, significantly enhances the efficacy of anticancer therapies through lysosomal dysfunction. This study underscores the critical role of lysosomal function modulated by amino acid metabolism in GBM pathogenesis and treatment.

  2. Mitochondria in Lung Cancer Progression

    Masafumi Noguchi, Keiko Iwata, Norihito Shintani, Atsuko Kasahara

    Current Pharmacology Reports　2024/08/27

    Publisher: Springer Science and Business Media LLC

    DOI： 10.1007/s40495-024-00361-3 　

    eISSN： 2198-641X

  3. A Supramolecular Biosensor for Rapid and High-Throughput Quantification of a Disease-Associated Niacin Metabolite Peer-reviewed

    Masaya Ueno, Hiroki Sugiyama, Feng Li, Tatsuya Nishimura, Hiroshi Arakawa, Xi Chen, Xiaoxiao Cheng, Shinji Takeuchi, Yumie Takeshita, Toshinari Takamura, Sakae Miyagi, Tadashi Toyama, Tomoyoshi Soga, Yusuke Masuo, Yukio Kato, Hiroyuki Nakamura, Hiromasa Tsujiguchi, Akinori Hara, Atsushi Tajima, Moeko Noguchi-Shinohara, Kenjiro Ono, Kenta Kurayoshi, Masahiko Kobayashi, Yuko Tadokoro, Atsuko Kasahara, Mahmoud I. Shoulkamy, Katsuhiro Maeda, Tomoki Ogoshi, Atsushi Hirao

    Analytical Chemistry　96　(36)　14499-14507　2024/08/26

    Publisher: American Chemical Society (ACS)

    DOI： 10.1021/acs.analchem.4c02653 　

    ISSN： 0003-2700

    eISSN： 1520-6882

  4. Targeting cis-regulatory elements of FOXO family is a novel therapeutic strategy for induction of leukemia cell differentiation. International-journal Peer-reviewed

    Kenta Kurayoshi, Yusuke Takase, Masaya Ueno, Kumiko Ohta, Kyoko Fuse, Shuji Ikeda, Takayoshi Watanabe, Yuki Nishida, Shin-Ichi Horike, Kazuyoshi Hosomichi, Yuichi Ishikawa, Yuko Tadokoro, Masahiko Kobayashi, Atsuko Kasahara, Yongwei Jing, Mahmoud I Shoulkamy, Makiko Meguro-Horike, Kensuke Kojima, Hitoshi Kiyoi, Hiroshi Sugiyama, Hiroki Nagase, Atsushi Tajima, Atsushi Hirao

    Cell Death & Disease　14　(9)　642　2023/09

    DOI： 10.1038/s41419-023-06168-2 　

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    Differentiation therapy has been proposed as a promising therapeutic strategy for acute myeloid leukemia (AML); thus, the development of more versatile methodologies that are applicable to a wide range of AML subtypes is desired. Although the FOXOs transcription factor represents a promising drug target for differentiation therapy, the efficacy of FOXO inhibitors is limited in vivo. Here, we show that pharmacological inhibition of a common cis-regulatory element of forkhead box O (FOXO) family members successfully induced cell differentiation in various AML cell lines. Through gene expression profiling and differentiation marker-based CRISPR/Cas9 screening, we identified TRIB1, a complement of the COP1 ubiquitin ligase complex, as a functional FOXO downstream gene maintaining an undifferentiated status. TRIB1 is direct target of FOXO3 and the FOXO-binding cis-regulatory element in the TRIB1 promoter, referred to as the FOXO-responsive element in the TRIB1 promoter (FRE-T), played a critical role in differentiation blockade. Thus, we designed a DNA-binding pharmacological inhibitor of the FOXO-FRE-T interface using pyrrole-imidazole polyamides (PIPs) that specifically bind to FRE-T (FRE-PIPs). The FRE-PIPs conjugated to chlorambucil (FRE-chb) inhibited transcription of TRIB1, causing differentiation in various AML cell lines. FRE-chb suppressed the formation of colonies derived from AML cell lines but not from normal counterparts. Administration of FRE-chb inhibited tumor progression in vivo without remarkable adverse effects. In conclusion, targeting cis-regulatory elements of the FOXO family is a promising therapeutic strategy that induces AML cell differentiation.

  5. Inhibition of the mitochondria-shaping protein Opa1 restores sensitivity to Gefitinib in a lung adenocarcinomaresistant cell line. International-journal

    Masafumi Noguchi, Susumu Kohno, Anna Pellattiero, Yukino Machida, Keitaro Shibata, Norihito Shintani, Takashi Kohno, Noriko Gotoh, Chiaki Takahashi, Atsushi Hirao, Luca Scorrano, Atsuko Kasahara

    Cell death & disease　14　(4)　241-241　2023/04/05

    DOI： 10.1038/s41419-023-05768-2 　

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    Drug resistance limits the efficacy of chemotherapy and targeted cancer treatments, calling for the identification of druggable targets to overcome it. Here we show that the mitochondria-shaping protein Opa1 participates in resistance against the tyrosine kinase inhibitor gefitinib in a lung adenocarcinoma cell line. Respiratory profiling revealed that oxidative metabolism was increased in this gefitinib-resistant lung cancer cell line. Accordingly, resistant cells depended on mitochondrial ATP generation, and their mitochondria were elongated with narrower cristae. In the resistant cells, levels of Opa1 were increased and its genetic or pharmacological inhibition reverted the mitochondrial morphology changes and sensitized them to gefitinib-induced cytochrome c release and apoptosis. In vivo, the size of gefitinib-resistant lung orthotopic tumors was reduced when gefitinib was combined with the specific Opa1 inhibitor MYLS22. The combo gefitinib-MYLS22 treatment increased tumor apoptosis and reduced its proliferation. Thus, the mitochondrial protein Opa1 participates in gefitinib resistance and can be targeted to overcome it.

  6. RHEB is a potential therapeutic target in T cell acute lymphoblastic leukemia

    Loc Thi Pham, Hui Peng, Masaya Ueno, Susumu Kohno, Atuso Kasada, Kazuyoshi Hosomichi, Takehiro Sato, Kenta Kurayoshi, Masahiko Kobayashi, Yuko Tadokoro, Atsuko Kasahara, Mahmoud I. Shoulkamy, Bo Xiao, Paul F. Worley, Chiaki Takahashi, Atsushi Tajima, Atsushi Hirao

    Biochemical and Biophysical Research Communications　621　74-79　2022/09

    Publisher: Elsevier BV

    DOI： 10.1016/j.bbrc.2022.06.089 　

    ISSN： 0006-291X

  7. Therapeutic advantage of targeting lysosomal membrane integrity supported by lysophagy in malignant glioma. International-journal

    Yongwei Jing, Masahiko Kobayashi, Ha Thi Vu, Atsuko Kasahara, Xi Chen, Loc Thi Pham, Kenta Kurayoshi, Yuko Tadokoro, Masaya Ueno, Tomoki Todo, Mitsutoshi Nakada, Atsushi Hirao

    Cancer science　113　(8)　2716-2726　2022/08

    DOI： 10.1111/cas.15451 　

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    Lysosomes function as the digestive system of a cell and are involved in macromolecular recycling, vesicle trafficking, metabolic reprogramming, and progrowth signaling. Although quality control of lysosome biogenesis is thought to be a potential target for cancer therapy, practical strategies have not been established. Here, we show that lysosomal membrane integrity supported by lysophagy, a selective autophagy for damaged lysosomes, is a promising therapeutic target for glioblastoma (GBM). In this study, we found that ifenprodil, an FDA-approved drug with neuromodulatory activities, efficiently inhibited spheroid formation of patient-derived GBM cells in a combination with autophagy inhibition. Ifenprodil increased intracellular Ca2+ level, resulting in mitochondrial reactive oxygen species-mediated cytotoxicity. The ifenprodil-induced Ca2+ elevation was due to Ca2+ release from lysosomes, but not endoplasmic reticulum, associated with galectin-3 punctation as an indicator of lysosomal membrane damage. As the Ca2+ release was enhanced by ATG5 deficiency, autophagy protected against lysosomal membrane damage. By comparative analysis of 765 FDA-approved compounds, we identified another clinically available drug for central nervous system (CNS) diseases, amoxapine, in addition to ifenprodil. Both compounds promoted degradation of lysosomal membrane proteins, indicating a critical role of lysophagy in quality control of lysosomal membrane integrity. Importantly, a synergistic inhibitory effect of ifenprodil and chloroquine, a clinically available autophagy inhibitor, on spheroid formation was remarkable in GBM cells, but not in nontransformed neural progenitor cells. Finally, chloroquine dramatically enhanced effects of the compounds inducing lysosomal membrane damage in a patient-derived xenograft model. These data demonstrate a therapeutic advantage of targeting lysosomal membrane integrity in GBM.

  8. Essential role of autophagy in protecting neonatal haematopoietic stem cells from oxidative stress in a p62-independent manner. International-journal

    Naho Nomura, Chiaki Ito, Takako Ooshio, Yuko Tadokoro, Susumu Kohno, Masaya Ueno, Masahiko Kobayashi, Atsuko Kasahara, Yusuke Takase, Kenta Kurayoshi, Sha Si, Chiaki Takahashi, Masaaki Komatsu, Toru Yanagawa, Atsushi Hirao

    Scientific reports　11　(1)　1666-1666　2021/01/18

    DOI： 10.1038/s41598-021-81076-z 　

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    Autophagy is a cellular degradation system contributing to homeostasis of tissue stem cells including haematopoietic stem cells (HSCs). It plays pleiotropic roles in HSC characteristics throughout life, but its stage-specific roles in HSC self-renewal are unclear. To investigate the effects of Atg5 deletion on stage-specific HSC functions, we compared the repopulating capacity of HSCs in Atg5f/f;Vavi-cre mice from postnatal day (P) 0-7 weeks of age. Interestingly, Atg5 deficiency led to no remarkable abnormality in the HSC self-renewal capacity at P0, but significant defects at P7, followed by severe defects. Induction of Atg5 deletion at P5 by tamoxifen administration to Atg5f/f;Rosa26-Cre-ERT2 mice resulted in normal haematopoiesis, including the HSC population, until around 1 year, suggesting that Atg5 in the early neonatal period was critical for haematopoiesis in adults. Mitochondrial oxidative stress was increased by Atg5 loss in neonatal HSC/progenitor cells. Although p62 had accumulated in immature bone marrow cells of Atg5f/f;Vavi-cre mice, p62 deletion did not restore defective HSC functions, indicating that Atg5-dependent haematopoietic regulation in the developmental period was independent of p62. This study proposes a critical role of autophagy in HSC protection against harsh environments in the early neonatal stage, which is essential for healthy long-term haematopoiesis.

  9. Pillar[6]arene acts as a biosensor for quantitative detection of a vitamin metabolite in crude biological samples

    Masaya Ueno, Takuya Tomita, Hiroshi Arakawa, Takahiro Kakuta, Tada-aki Yamagishi, Jumpei Terakawa, Takiko Daikoku, Shin-ichi Horike, Sha Si, Kenta Kurayoshi, Chiaki Ito, Atsuko Kasahara, Yuko Tadokoro, Masahiko Kobayashi, Tsutomu Fukuwatari, Ikumi Tamai, Atsushi Hirao, Tomoki Ogoshi

    Communications Chemistry　3　(1)　2020/12

    Publisher: Springer Science and Business Media LLC

    DOI： 10.1038/s42004-020-00430-w 　

    eISSN： 2399-3669

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    <title>Abstract</title>Metabolic syndrome is associated with obesity, hypertension, and dyslipidemia, and increased cardiovascular risk. Therefore, quick and accurate measurements of specific metabolites are critical for diagnosis; however, detection methods are limited. Here we describe the synthesis of pillar[n]arenes to target 1-methylnicotinamide (1-MNA), which is one metabolite of vitamin B3 (nicotinamide) produced by the cancer-associated nicotinamide <italic>N</italic>-methyltransferase (NNMT). We found that water-soluble pillar[5]arene (P5A) forms host–guest complexes with both 1-MNA and nicotinamide, and water-soluble pillar[6]arene (P6A) selectively binds to 1-MNA at the micromolar level. P6A can be used as a “turn-off sensor” by photoinduced electron transfer (detection limit is 4.38 × 10−6 M). In our cell-free reaction, P6A is used to quantitatively monitor the activity of NNMT. Moreover, studies using NNMT-deficient mice reveal that P6A exclusively binds to 1-MNA in crude urinary samples. Our findings demonstrate that P6A can be used as a biosensor to quantify 1-MNA in crude biological samples.

  10. Autophagy inhibition synergizes with calcium mobilization to achieve efficient therapy of malignant gliomas. International-journal Peer-reviewed

    Ha Thi Vu, Masahiko Kobayashi, Ahmed M Hegazy, Yuko Tadokoro, Masaya Ueno, Atsuko Kasahara, Yusuke Takase, Naho Nomura, Hui Peng, Chiaki Ito, Yasushi Ino, Tomoki Todo, Mitsutoshi Nakada, Atsushi Hirao

    Cancer science　109　(8)　2497-2508　2018/08

    DOI： 10.1111/cas.13695 　

    ISSN： 1347-9032

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    Autophagy plays a critical role in tumorigenesis, but how autophagy contributes to cancer cells' responses to chemotherapeutics remains controversial. To investigate the roles of autophagy in malignant gliomas, we used CRISPR/CAS9 to knock out the ATG5 gene, which is essential for autophagosome formation, in tumor cells derived from patients with glioblastoma. While ATG5 disruption inhibited autophagy, it did not change the phenotypes of glioma cells and did not alter their sensitivity to temozolomide, an agent used for glioblastoma patient therapy. Screening of an anticancer drug library identified compounds that showed greater efficacy to ATG5-knockout glioma cells compared to control. While several selected compounds, including nigericin and salinomycin, remarkably induced autophagy, potent autophagy inducers by mTOR inhibition did not exhibit the ATG5-dependent cytoprotective effects. Nigericin in combination with ATG5 deficiency synergistically suppressed spheroid formation by glioma cells in a manner mitigated by Ca2+ chelation or CaMKK inhibition, indicating that, in combination with autophagy inhibition, calcium-mobilizing compounds contribute to efficient anticancer therapeutics. ATG5-knockout cells treated with nigericin showed increased mitochondria-derived reactive oxygen species and apoptosis compared to controls, indicating that autophagy protects glioma cells from mitochondrial reactive oxygen species-mediated damage. Finally, using a patient-derived xenograft model, we demonstrated that chloroquine, a pharmacological autophagy inhibitor, dramatically enhanced the efficacy of compounds selected in this study. Our findings propose a novel therapeutic strategy in which calcium-mobilizing compounds are combined with autophagy inhibitors to treat patients with glioblastoma.

  11. Mitochondrial dynamics coordinate cell differentiation Peer-reviewed

    Masafumi Noguchi, Atsuko Kasahara

    Biochemical and Biophysical Research Communications　500　(1)　59-64　2018/05/27

    Publisher: Elsevier B.V.

    DOI： 10.1016/j.bbrc.2017.06.094 　

    ISSN： 1090-2104 0006-291X

  12. ER-mitochondria contacts control surface glycan expression and sensitivity to killer lymphocytes in glioma stem-like cells Peer-reviewed

    Esen Yonca Bassoy, Atsuko Kasahara, Valentina Chiusolo, Guillaume Jacquemin, Emma Boydell, Sebastian Zamorano, Cristina Riccadonna, Serena Pellegatta, Nicolas Hulo, Valerie Dutoit, Madiha Derouazi, Pierre Yves Dietrich, Paul R. Walker, Denis Martinvalet

    EMBO JOURNAL　36　(11)　1493-1512　2017/06

    DOI： 10.15252/embj.201695429 　

    ISSN： 0261-4189

    eISSN： 1460-2075

  13. Granzyme B-induced mitochondrial ROS are required for apoptosis Peer-reviewed

    G. Jacquemin, D. Margiotta, A. Kasahara, E. Y. Bassoy, M. Walch, J. Thiery, J. Lieberman, D. Martinvalet

    CELL DEATH AND DIFFERENTIATION　22　(5)　862-874　2015/04

    DOI： 10.1038/cdd.2014.180 　

    ISSN： 1350-9047

    eISSN： 1476-5403

  14. Mitochondria: from cell death executioners to regulators of cell differentiation Peer-reviewed

    Atsuko Kasahara, Luca Scorrano

    TRENDS IN CELL BIOLOGY　24　(12)　761-770　2014/12

    DOI： 10.1016/j.tcb.2014.08.005 　

    ISSN： 0962-8924

  15. Mitochondrial fusion directs cardiomyocyte differentiation via calcineurin and Notch signaling. Peer-reviewed

    Kasahara A, Cipolat S, Chen Y, Dorn GW, Scorrano L

    Science (New York, N.Y.)　342　(6159)　734-737　2013/11

    DOI： 10.1126/science.1241359 　

    ISSN： 0036-8075

  16. Normal mitochondrial respiratory function is essential for spatial remote memory in mice Peer-reviewed

    Daisuke Tanaka, Kazuto Nakada, Keizo Takao, Emi Ogasawara, Atsuko Kasahara, Akitsugu Sato, Hiromichi Yonekawa, Tsuyoshi Miyakawa, Jun-Ichi Hayashi

    MOLECULAR BRAIN　1　21　2008

    DOI： 10.1186/1756-6606-1-21 　

    ISSN： 1756-6606

  17. Deletion-mutant mtDNA increases in somatic tissues but decreases in female germ cells with age Peer-reviewed

    Akitsugu Sato, Kazuto Nakada, Hiroshi Shitara, Atsuko Kasahara, Hiromichi Yonekawa, Jun-Ichi Hayashi

    GENETICS　177　(4)　2031-2037　2007/12

    DOI： 10.1534/genetics.107.081026 　

    ISSN： 0016-6731

  18. [Mutagens inducing mutations in mammalian mitochondrial DNA]. Peer-reviewed

    Watanabe N, Kasahara A, Nakada K, Hayashi J

    Nihon rinsho. Japanese journal of clinical medicine　60 Suppl 4　35-38　2002/04

    ISSN： 0047-1852

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Misc. 7

  1. Generation of trans-mitochondrial mice carrying homoplasmic mtDNA with a missense mutation in a structural gene using ES cells

    Atsuko Kasahara, Jun-Ichi Hayashi

    NEUROMUSCULAR DISORDERS　16　S58-S58　2006/07

    ISSN： 0960-8966

  2. Generation of trans-mitochondrial mice carrying homoplasmic mtDNAs with a missense mutation in a structural gene using ES cells International-journal

    A Kasahara, K Ishikawa, M Yamaoka, M Ito, N Watanabe, M Akimoto, A Sato, K Nakada, H Endo, Y Suda, S Aizawa, JI Hayashi

    HUMAN MOLECULAR GENETICS　15　(6)　871-881　2006/03

    DOI： 10.1093/hmg/ddl005 　

    ISSN： 0964-6906

  3. Generation of trans-mitochondrial mice carrying homoplasmic mtDNAs with a missense mutation in a structural gene using ES cells

    A Kasahara, K Ishikawa, M Yamaoka, M Ito, N Watanabe, M Akimoto, A Sato, K Nakada, H Endo, Y Suda, S Aizawa, JI Hayashi

    HUMAN MOLECULAR GENETICS　15　(6)　871-881　2006/03

    DOI： 10.1093/hmg/ddl005 　

    ISSN： 0964-6906

  4. Application of ES cells for generation of respiration-deficient mice carrying mtDNA with a large-scale deletion International-journal

    K Ishikawa, A Kasahara, N Watanabe, K Nakada, A Sato, Y Suda, S Aizawa, JI Hayashi

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　333　(2)　590-595　2005/07

    DOI： 10.1016/j.bbrc.2005.05.155 　

    ISSN： 0006-291X

  5. Application of ES cells for generation of respiration-deficient mice carrying mtDNA with a large-scale deletion

    K Ishikawa, A Kasahara, N Watanabe, K Nakada, A Sato, Y Suda, S Aizawa, JI Hayashi

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　333　(2)　590-595　2005/07

    DOI： 10.1016/j.bbrc.2005.05.155 　

    ISSN： 0006-291X

  6. Accumulation of pathogenic Delta mtDNA induced deafness but not diabetic phenotypes in mito-mice

    K Nakada, A Sato, H Sone, A Kasahara, K Ikeda, Y Kagawa, H Yonekawa, J Hayashi

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　323　(1)　175-184　2004/10

    DOI： 10.1016/j.bbrc.2004.08.073 　

    ISSN： 0006-291X

  7. Accumulation of pathogenic Delta mtDNA induced deafness but not diabetic phenotypes in mito-mice

    K Nakada, A Sato, H Sone, A Kasahara, K Ikeda, Y Kagawa, H Yonekawa, J Hayashi

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　323　(1)　175-184　2004/10

    DOI： 10.1016/j.bbrc.2004.08.073 　

    ISSN： 0006-291X

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Research Projects 5

  1. 細胞運命決定におけるオルガネラ接触部位制御メカニズムの解明

    笠原 敦子

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 基盤研究(C)

    Institution: 東北大学

    2024/04/01 - 2027/03/31

  2. Exploring the role of mitochondrial dynamics in cancer stemless

    KASAHARA Atsuko

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (C)

    Institution: Kanazawa University

    2019/04/01 - 2022/03/31

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    The purpose of this study was to understand how “mitochondria-shaping proteins” could be involved in the malignant phenotypes of cancer cells. Gefitinib-resistance lung adenocarcinoma cells maintain their resistance by mitochondrial inner membrane profusion factor OPA1 up-regulation, and down-regulation or pharmacological inhibition of OPA1 restore their gefitinib resistance. Prostate cancer cells display different calcium regulation upon mitochondrial shape alteration compared to healthy prostate cells. It was unsuccessful in identifying the upstream regulators to control the expression of “mitochondria-shaping” proteins that contribute to the malignant phenotypes.

  3. Exploring the mitochondrial retrograde control in malignant progression

    KASAHARA Atsuko

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Young Scientists (B)

    Institution: Kanazawa University

    2017/04/01 - 2019/03/31

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    Glioblastoma (GBM) is a very aggressive and destructive brain tumour. Numerous studies have identified a tumour cell population in GBM that can initiate glioma development, as glioma stem-like cells. We observed the specific mitochondrial shape, and intracellular localisation in glioma stem-like cells, that regulates sialylated glycan expressions at the plasma membrane, which directly influences the physiological contact, and killing efficiency of cytotoxic T lymphocyte to the glioma stem-like cells.

  4. ‐ Competitive

  5. - Competitive