2023/06/01 更新

ハマノ モモコ
濱野 桃子
HAMANO Momoko
Scopus 論文情報  
総論文数: 0  総Citation: 0  h-index: 5

Citation Countは当該年に発表した論文の被引用数

所属
大学院情報工学研究院 生命化学情報工学研究系
職名
助教
外部リンク

取得学位

  • 九州大学  -  博士(農学)   2019年03月

学内職務経歴

  • 2020年10月 - 現在   九州工業大学   大学院情報工学研究院   生命化学情報工学研究系     助教

論文

  • TRANSDIRE: data-driven direct reprogramming by a pioneer factor-guided trans-omics approach 査読有り 国際誌

    Ryohei Eguchi, Momoko Hamano, Michio Iwata, Toru Nakamura, Shinya Oki, Yoshihiro Yamanishi

    Bioinformatics   38 ( 10 )   2839 - 2846   2022年04月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)

    Motivation: Direct reprogramming involves the direct conversion of fully differentiated mature cell types into various other cell types while bypassing an intermediate pluripotent state (e.g. induced pluripotent stem cells). Cell differentiation by direct reprogramming is determined by two types of transcription factors (TFs): Pioneer factors (PFs) and cooperative TFs. PFs have the distinct ability to open chromatin aggregations, assemble a collective of cooperative TFs and activate gene expression. The experimental determination of two types of TFs is extremely difficult and costly. Results: In this study, we developed a novel computational method, TRANSDIRE (TRANS-omics-based approach for DIrect REprogramming), to predict the TFs that induce direct reprogramming in various human cell types using multiple omics data. In the algorithm, potential PFs were predicted based on low signal chromatin regions, and the cooperative TFs were predicted through a trans-omics analysis of genomic data (e.g. enhancers), transcriptome data (e.g. gene expression profiles in human cells), epigenome data (e.g. chromatin immunoprecipitation sequencing data) and interactome data. We applied the proposed methods to the reconstruction of TFs that induce direct reprogramming from fibroblasts to six other cell types: Hepatocytes, cartilaginous cells, neurons, cardiomyocytes, pancreatic cells and Paneth cells. We demonstrated that the methods successfully predicted TFs for most cell conversions with high accuracy. Thus, the proposed methods are expected to be useful for various practical applications in regenerative medicine.

    DOI: 10.1093/bioinformatics/btac209

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  • Prediction of single-cell mechanisms for disease progression in hypertrophic remodelling by a trans-omics approach 査読有り

    Hamano M., Nomura S., Iida M., Komuro I., Yamanishi Y.

    Scientific reports   11 ( 1 )   2021年04月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)

    Heart failure is a heterogeneous disease with multiple risk factors and various pathophysiological types, which makes it difficult to understand the molecular mechanisms involved. In this study, we proposed a trans-omics approach for predicting molecular pathological mechanisms of heart failure and identifying marker genes to distinguish heterogeneous phenotypes, by integrating multiple omics data including single-cell RNA-seq, ChIP-seq, and gene interactome data. We detected a significant increase in the expression level of natriuretic peptide A (Nppa), after stress loading with transverse aortic constriction (TAC), and showed that cardiomyocytes with high Nppa expression displayed specific gene expression patterns. Multiple NADH ubiquinone complex family, which are associated with the mitochondrial electron transport system, were negatively correlated with Nppa expression during the early stages of cardiac hypertrophy. Large-scale ChIP-seq data analysis showed that Nkx2-5 and Gtf2b were transcription factors characteristic of high-Nppa-expressing cardiomyocytes. Nppa expression levels may, therefore, represent a useful diagnostic marker for heart failure.

    DOI: 10.1038/s41598-021-86821-y

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  • TEAD1 trapping by the Q353R–Lamin A/C causes dilated cardiomyopathy 査読有り 国際誌

    Shintaro Yamada, Toshiyuki Ko, Masamichi Ito, Tatsuro Sassa, Seitaro Nomura, Hiromichi Okuma, Mayuko Sato, Tsuyoshi Imasaki, Satoshi Kikkawa, Bo Zhang, Takanobu Yamada, Yuka Seki, Kanna Fujita, Manami Katoh, Masayuki Kubota, Satoshi Hatsuse, Mikako Katagiri, Hiromu Hayashi, Momoko Hamano, Norifumi Takeda, Hiroyuki Morita, Shuji Takada, Masashi Toyoda, Masanobu Uchiyama, Masashi Ikeuchi, Kiminori Toyooka, Akihiro Umezawa, Yoshihiro Yamanishi, Ryo Nitta, Hiroyuki Aburatani, Issei Komuro

    Science Advances   2023年04月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)

  • Reciprocal expression of the immune response genes CXCR3 and IFI44L as module hubs are associated with patient survivals in primary central nervous system lymphoma 査読有り

    Takashima Y., Hamano M., Yoshii K., Hayano A., Fukai J., Iwadate Y., Kajiwara K., Hondoh H., Yamanaka R.

    International Journal of Clinical Oncology   28 ( 3 )   468 - 481   2023年03月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)

    Purpose: Here, we investigated expression modules reflecting the reciprocal expression of the cancer microenvironment and immune response-related genes associated with poor prognosis in primary central nervous system lymphoma (PCNSL). Methods: Weighted gene coexpression network analysis revealed representative modules, including neurogenesis, immune response, anti-virus, microenvironment, gene expression and translation, extracellular matrix, morphogenesis, and cell adhesion in the transcriptome data of 31 PCNSL samples. Results : Gene expression networks were also reflected by protein–protein interaction networks. In particular, some of the hub genes were highly expressed in patients with PCNSL with prognoses as follows: AQP4, SLC1A3, GFAP, CXCL9, CXCL10, GBP2, IFI6, OAS2, IFIT3, DCN, LRP1, and LUM with good prognosis; and STAT1, IFITM3, GZMB, ISG15, LY6E, TGFB1, PLAUR, MMP4, FTH1, PLAU, CSF3R, FGR, POSTN, CCR7, TAS1R3, small ribosomal subunit genes, and collagen type 1/3/4/6 genes with poor prognosis. Furthermore, prognosis prediction formulae were constructed using the Cox proportional-hazards regression model, which demonstrated that the IP-10 receptor gene CXCR3 and type I interferon-induced protein gene IFI44L could predict patient survival in PCNSL. Conclusion: These results indicate that the differential expression and balance of immune response and microenvironment genes may be required for PCNSL tumor growth or prognosis prediction, which would help understanding the mechanism of tumorigenesis and potential therapeutic targets in PCNSL.

    DOI: 10.1007/s10147-022-02285-8

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  • Small compound-based direct cell conversion with combinatorial optimization of pathway regulations 査読有り 国際誌

    Toru Nakamura, Michio Iwata, Momoko Hamano, Ryohei Eguchi, Jun-ichi Takeshita and Yoshihiro Yamanishi

    Bioinformatics ( Bioinformatics )   38 ( 2 )   ii99 - ii105   2022年09月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)

    MOTIVATION: Direct cell conversion, direct reprogramming (DR), is an innovative technology that directly converts source cells to target cells without bypassing induced pluripotent stem cells. The use of small compounds (e.g. drugs) for DR can help avoid carcinogenic risk induced by gene transfection; however, experimentally identifying small compounds remains challenging because of combinatorial explosion. RESULTS: In this article, we present a new computational method, COMPRENDRE (combinatorial optimization of pathway regulations for direct reprograming), to elucidate the mechanism of small compound-based DR and predict new combinations of small compounds for DR. We estimated the potential target proteins of DR-inducing small compounds and identified a set of target pathways involving DR. We identified multiple DR-related pathways that have not previously been reported to induce neurons or cardiomyocytes from fibroblasts. To overcome the problem of combinatorial explosion, we developed a variant of a simulated annealing algorithm to identify the best set of compounds that can regulate DR-related pathways. Consequently, the proposed method enabled to predict new DR-inducing candidate combinations with fewer compounds and to successfully reproduce experimentally verified compounds inducing the direct conversion from fibroblasts to neurons or cardiomyocytes. The proposed method is expected to be useful for practical applications in regenerative medicine. AVAILABILITY AND IMPLEMENTATION: The code supporting the current study is available at the http://labo.bio.kyutech.ac.jp/~yamani/comprendre. SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.

    DOI: 10.1093/bioinformatics/btac475

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  • Small compound-based direct cell conversion with combinatorial optimization of pathway regulations 査読有り 国際誌

    Toru Nakamura, Michio Iwata, Momoko Hamano, Ryohei Eguchi, Jun-ichi Takeshita, Yoshihiro Yamanishi

    Bioinformatics ( Bioinformatics )   2022年09月

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    記述言語:英語   掲載種別:研究論文(国際会議プロシーディングス)

  • Hepatocyte-specific phgdh-deficient mice culminate in mild obesity, insulin resistance, and enhanced vulnerability to protein starvation 招待有り 査読有り

    Hamano M., Esaki K., Moriyasu K., Yasuda T., Mohri S., Tashiro K., Hirabayashi Y., Furuya S.

    Nutrients   13 ( 10 )   2021年10月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)

    L-Serine (Ser) is synthesized de novo from 3-phosphoglycerate via the phosphorylated pathway committed by phosphoglycerate dehydrogenase (Phgdh). A previous study reported that feeding a protein-free diet increased the enzymatic activity of Phgdh in the liver and enhanced Ser synthesis in the rat liver. However, the nutritional and physiological functions of Ser synthesis in the liver remain unclear. To clarify the physiological significance of de novo Ser synthesis in the liver, we generated liver hepatocyte-specific Phgdh KO (LKO) mice using an albumin-Cre driver. The LKO mice exhibited a significant gain in body weight compared to Floxed controls at 23 weeks of age and impaired systemic glucose metabolism, which was accompanied by diminished insu-lin/IGF signaling. Although LKO mice had no apparent defects in steatosis, the molecular signatures of inflammation and stress responses were evident in the liver of LKO mice. Moreover, LKO mice were more vulnerable to protein starvation than the Floxed mice. These observations demonstrate that Phgdh-dependent de novo Ser synthesis in liver hepatocytes contributes to the maintenance of systemic glucose tolerance, suppression of inflammatory response, and resistance to protein starva-tion.

    DOI: 10.3390/nu13103468

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  • Transcriptional activation of chac1 and other atf4-target genes induced by extracellular l-serine depletion is negated with glycine consumption in hepa1-6 hepatocarcinoma cells 査読有り

    Hamano M., Tomonaga S., Osaki Y., Oda H., Kato H., Furuya S.

    Nutrients   12 ( 10 )   1 - 11   2020年10月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)

    © 2020 by the authors. Licensee MDPI, Basel, Switzerland. Mouse embryonic fibroblasts lacking D-3-phosphoglycerate dehydrogenase (Phgdh), which catalyzes the first step of de novo synthesis of l-serine, are particularly sensitive to depletion of extracellular L-serine. In these cells, depletion of l-serine leads to a rapid reduction of intracellular L-serine, cell growth arrest, and altered expression of a wide variety of genes. However, it remains unclear whether reduced availability of extracellular l-serine elicits such responses in other cell types expressing Phgdh. Here, we show in the mouse hepatoma cell line Hepa1-6 that extracellular l-serine depletion transiently induced transcriptional activation of Atf4-target genes, including cation transport regulator-like protein 1 (Chac1). Expression levels of these genes returned to normal 24 h after l-serine depletion, and were suppressed by the addition of l-serine or glycine in the medium. Extracellular l-serine depletion caused a reduction of extracellular and intracellular glycine levels but maintained intracellular l-serine levels in the cells. Further, Phgdh and serine hydroxymethyltransferase 2 (Shmt2) were upregulated after l-serine depletion. These results led us to conclude that the Atf4-mediated gene expression program is activated by extracellular l-serine depletion in Hepa1-6 cells expressing Phgdh, but is antagonized by the subsequent upregulation of l-serine synthesis, mainly from autonomous glycine consumption.

    DOI: 10.3390/nu12103018

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  • GSEA-assisted gene signatures valid for combinations of prognostic markers in PCNSL 査読有り 国際誌

    Takashima Y., Hamano M., Fukai J., Iwadate Y., Kajiwara K., Kobayashi T., Hondoh H., Yamanaka R.

    Scientific Reports   10 ( 1 )   2020年05月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)

    Primary central nervous system lymphoma (PCNSL) is a brain malignant non-Hodgkin’s B-cell lymphoma. The standard treatments are high-dose methotrexate (MTX)-based chemotherapies and deferred whole brain radiotherapy. However, MTX resistance-dependent global expression and signaling pathway changes and their relationship with prognoses have not yet been elucidated. Here, we conducted a global expression analysis with next-generation sequencing and gene set enrichment analysis (GSEA) in MTX-resistant PCNSL cell lines (HKBML-MTX and TK-MTX) and PCNSL tissues. In rank scores, genes listed in HKBML-MTX and TK-MTX were enriched in PCNSL with poor prognoses. In fold changes, a part of differentially-expressed genes in PCNSL tissues were also detected in HKBML-MTX and TK-MTX cells; FOXD2-AS1 and MMP19 were commonly expressed in both HKBML-MTX and TK-MTX, FABP5 and CD70 were HKBML-MTX-specifically expressed, and CLCN2, HOXB9, INE1, and LRP5L were TK-MTX-specifically expressed, which may provide a combination of prognostic markers on MTX-sensitivities in PCNSL. Additionally, PCNSL subgroups, divided with hierarchical clustering and Kaplan-Meier methods, included twenty commonly expressed genes in both HKBML-MTX and TK-MTX, ten HKBML-MTX-specifically expressed genes, and two TK-MTX-specifically expressed genes. These results suggest that the GSEA-assisted gene signatures can provide a combination for prognostic markers in recurrent PCNSL with MTX resistances.

    DOI: 10.1038/s41598-020-65463-6

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  • Predicting drug-induced transcriptome responses of a wide range of human cell lines by a novel tensor-train decomposition algorithm 査読有り

    Iwata M., Yuan L., Zhao Q., Tabei Y., Berenger F., Sawada R., Akiyoshi S., Hamano M., Yamanishi Y.

    Bioinformatics   35 ( 14 )   i191 - i199   2019年07月

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    記述言語:英語   掲載種別:研究論文(国際会議プロシーディングス)

    Motivation: Genome-wide identification of the transcriptomic responses of human cell lines to drug treatments is a challenging issue in medical and pharmaceutical research. However, drug-induced gene expression profiles are largely unknown and unobserved for all combinations of drugs and human cell lines, which is a serious obstacle in practical applications. Results: Here, we developed a novel computational method to predict unknown parts of drug-induced gene expression profiles for various human cell lines and predict new drug therapeutic indications for a wide range of diseases. We proposed a tensor-train weighted optimization (TT-WOPT) algorithm to predict the potential values for unknown parts in tensor-structured gene expression data. Our results revealed that the proposed TT-WOPT algorithm can accurately reconstruct drug-induced gene expression data for a range of human cell lines in the Library of Integrated Network-based Cellular Signatures. The results also revealed that in comparison with the use of original gene expression profiles, the use of imputed gene expression profiles improved the accuracy of drug repositioning. We also performed a comprehensive prediction of drug indications for diseases with gene expression profiles, which suggested many potential drug indications that were not predicted by previous approaches. Supplementary information: Supplementary data are available at Bioinformatics online.

    DOI: 10.1093/bioinformatics/btz313

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  • Enhanced vulnerability to oxidative stress and induction of inflammatory gene expression in 3-phosphoglycerate dehydrogenase-deficient fibroblasts 査読有り

    Hamano M., Haraguchi Y., Sayano T., Zyao C., Arimoto Y., Kawano Y., Moriyasu K., Udono M., Katakura Y., Ogawa T., Kato H., Furuya S.

    FEBS Open Bio   8 ( 6 )   914 - 922   2018年06月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)

    © 2018 The Authors. Published by FEBS Press and John Wiley & Sons Ltd. l-Serine (l-Ser) is a necessary precursor for the synthesis of proteins, lipids, glycine, cysteine, d-serine, and tetrahydrofolate metabolites. Low l-Ser availability activates stress responses and cell death; however, the underlying molecular mechanisms remain unclear. l-Ser is synthesized de novo from 3-phosphoglycerate with 3-phosphoglycerate dehydrogenase (Phgdh) catalyzing the first reaction step. Here, we show that l-Ser depletion raises intracellular H2O2 levels and enhances vulnerability to oxidative stress in Phgdh-deficient mouse embryonic fibroblasts. These changes were associated with reduced total glutathione levels. Moreover, levels of the inflammatory markers thioredoxin-interacting protein and prostaglandin-endoperoxide synthase 2 were upregulated under l-Ser-depleted conditions; this was suppressed by the addition of N-acetyl-l-cysteine. Thus, intracellular l-Ser deficiency triggers an inflammatory response via increased oxidative stress, and de novo l-Ser synthesis suppresses oxidative stress damage and inflammation when the external l-Ser supply is restricted.

    DOI: 10.1002/2211-5463.12429

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  • Microarray data on altered transcriptional program of Phgdh-deficient mouse embryonic fibroblasts caused by L-serine depletion 査読有り 国際誌

    Momoko Hamano, Tomoko Sayano, Wataru Kusada, Hisanori Kato, Shigeki Furuya

    Data in Brief   7   1598 - 1601   2016年04月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)

    DOI: 10.1016/j.dib.2016.04.052

  • Adaptive response to l-serine deficiency is mediated by p38 MAPK activation via 1-deoxysphinganine in normal fibroblasts 査読有り

    Sayano T., Kawano Y., Kusada W., Arimoto Y., Esaki K., Hamano M., Udono M., Katakura Y., Ogawa T., Kato H., Hirabayashi Y., Furuya S.

    FEBS Open Bio   6 ( 4 )   303 - 316   2016年04月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)

    © 2016 Federation of European Biochemical Societies. Reduced availability of l-serine limits cell proliferation and leads to an adaptation to l-serine-deficient environment, the underlying molecular mechanism of which remain largely unexplored. Genetic ablation of 3-phosphoglycerate dehydrogenase (Phgdh), which catalyzes the first step of de novo l-serine synthesis, led to diminished cell proliferation and the activation of p38 MAPK and stress-activated protein kinase/Jun amino-terminal kinase in mouse embryonic fibroblasts under l-serine depletion. The resultant l-serine deficiency induced cyclin-dependent kinase inhibitor 1a (Cdkn1a; p21) expression, which was mediated by p38 MAPK. Survival of the Phgdh-deficient mouse embryonic fibroblasts was markedly reduced by p38 MAPK inhibition under l-serine depletion, whereas p38 MAPK could be activated by 1-deoxysphinganine, an atypical alanine-derived sphingoid base that was found to accumulate in l-serine-depleted mouse embryonic fibroblasts. These observations provide persuasive evidence that when the external l-serine supply is limited, l-serine synthesized de novo in proliferating cells serves as a metabolic gatekeeper to maintain cell survival and the functions necessary for executing cell cycle progression. Database: Gene Expression Omnibus, accession number GSE55687. Using 3-phosphoglycerate dehydrogenase (Phgdh)-deficient mouse embryonic fibroblasts, we explored l-serine deficiency. Cell proliferation was reduced, but Cdkn1a/p21 expression was induced, mediated by p38 MAPK. These observations suggest that when the external l-serine supply is limited, l-serine synthesized de novo in proliferating cells serves as a metabolic gatekeeper to maintain cell survival and the functions necessary for executing cell cycle progression.

    DOI: 10.1002/2211-5463.12038

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著書

  • ダイレクトリプログラミング : 再生医療の新展開

    江口凌平,濱野桃子,岩田通夫,中村透,山西芳裕(共著 ,  範囲: データ駆動型ダイレクトリプログラミング)

    株式会社エヌ・ティー・エヌ  2020年08月 

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    担当ページ:239-245   記述言語:日本語

担当授業科目(学内)

  • 2022年度   分子生物学