Updated on 2023/10/12

写真a

 
KISHIDA Michiko
 
Organization
Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area Graduate School of Medical and Dental Sciences Health Research Course Developmental Medicine Assistant Professor
Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area Faculty of Medicine
Title
Assistant Professor

Degree

  • 博士(医学) ( 2000.3   広島大学 )

Research Interests

  • シグナル伝達

Research Areas

  • Life Science / Cell biology

Research History

  • Kagoshima University

    2007.7

  • Kagoshima University   Assistant Professor

    2007.7

Professional Memberships

  • 日本癌学会

    2015.10

 

Papers

  • Ono Y., Fuchigami T., Kishida M., Koyama H., Iijima M., Oishi K., Kibe T., Ishihata K., Nishizawa Y., Kiyono T., Nakamura N., Kishida S. .  Interleukin-1α promotes matrix metalloproteinase-9 expression, cellular motility, and local invasiveness of ameloblastoma cells .  Oral Science International   2023.5

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    Language:Japanese   Publisher:Oral Science International  

    Aim: Although ameloblastoma is a benign tumor, its local invasiveness and recurrence rate are both high. Thus, the regulation of the invasiveness of ameloblastoma cells into the surrounding tissue is required to understand its pathogenesis. Ameloblastoma cells secrete several matrix metalloproteinases (MMPs); however, the factors inducing their secretion remain unclear. We previously suggested that interleukin (IL)-1α derived from ameloblastoma cells triggers the production of inflammatory cytokines by stromal fibroblasts. In this study, we estimated whether IL-1α affects the behavior of ameloblastoma cells. Methods: The gene expression of MMP-9 was assessed by real-time reverse transcription–polymerase chain reaction (RT-PCR). The secretion of MMP-9 was assessed by enzyme-linked immunosorbent assay (ELISA). The motility of AM-3 ameloblastoma and Raw264.7 (macrophage derived cells) cells and the invasiveness of AM-3 cells were calculated using the Boyden chamber. The invasiveness of AM-3 cells toward human foreskin fibroblast (HFF)-2 fibroblasts were assessed using modified double-layered collagen gel hemisphere (DL-CGH). Results: The mRNA expression and secretion of MMP-9 by AM-3 ameloblastoma cells were significantly increased by IL-1α stimulation. The motilities of AM-3 and RAW264.7 macrophage derived cells and the invasiveness of AM-3 cells were significantly enhanced by IL-1α and suppressed by an IL-1 receptor antagonist (IL-1Ra). The invasiveness of AM-3 cells towards HFF-2 fibroblasts in a DL-CGH model was suppressed by a treatment with IL-1Ra or an anti-IL-1α neutralizing antibody. Conclusion: IL-1α itself or the IL-1α-dependent production of unidentified chemo attractants by stromal cells may be important for the local invasiveness of ameloblastoma cells, and IL-1α might be a therapeutic target of the ameloblastoma.

    DOI: 10.1002/osi2.1193

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  • Betzler A.C., Strobel H., Abou Kors T., Ezić J., Lesakova K., Pscheid R., Azoitei N., Sporleder J., Staufenberg A.R., Drees R., Weissinger S.E., Greve J., Doescher J., Theodoraki M.N., Schuler P.J., Laban S., Kibe T., Kishida M., Kishida S., Idel C., Hoffmann T.K., Lavitrano M., Grassilli E., Brunner C. .  BTK Isoforms p80 and p65 Are Expressed in Head and Neck Squamous Cell Carcinoma (HNSCC) and Involved in Tumor Progression .  Cancers15 ( 1 )   2023.1

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    Language:Japanese   Publisher:Cancers  

    Here, we describe the expression of Bruton’s Tyrosine Kinase (BTK) in head and neck squamous cell carcinoma (HNSCC) cell lines as well as in primary HNSCC samples. BTK is a kinase initially thought to be expressed exclusively in cells of hematopoietic origin. Apart from the 77 kDa BTK isoform expressed in immune cells, particularly in B cells, we identified the 80 kDa and 65 kDa BTK isoforms in HNSCC, recently described as oncogenic. Importantly, we revealed that both isoforms are products of the same mRNA. By investigating the mechanism regulating oncogenic BTK-p80/p65 expression in HNSSC versus healthy or benign tissues, our data suggests that the epigenetic process of methylation might be responsible for the initiation of BTK-p80/p65 expression in HNSCC. Our findings demonstrate that chemical or genetic abrogation of BTK activity leads to inhibition of tumor progression in terms of proliferation and vascularization in vitro and in vivo. These observations were associated with cell cycle arrest and increased apoptosis and autophagy. Together, these data indicate BTK-p80 and BTK-p65 as novel HNSCC-associated oncogenes. Owing to the fact that abundant BTK expression is a characteristic feature of primary and metastatic HNSCC, targeting BTK activity appears as a promising therapeutic option for HNSCC patients.

    DOI: 10.3390/cancers15010310

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  • Chairani E.Chairani E, Fuchigami T, Koyama H, Ono Y, Iijima M, Kishida M, Kibe T, Nakamura N, Kishida S. .  Intercellular signaling between ameloblastoma and osteoblasts .  Biochemistry and Biophysics Reports30   101233   2022.2

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    Language:Japanese   Publisher:Biochemistry and Biophysics Reports  

    Ameloblastoma is an odontogenic tumor located in the bone jaw with clinical characteristics of extensive bone resorption. It is a locally invasive tumor with a high recurrence rate despite adequate surgical removal. In bone disease, tumors and other cells including osteoblasts, osteoclasts, and osteocytes in the bone microenvironment contribute to the pathogenesis of tumor growth. However, the effect of osteoblasts on ameloblastoma cells is not well-understood, and there has been limited research on interactions between them. This study investigated interactions between ameloblastoma cells and osteoblasts using a human ameloblastoma cell line (AM-3 ameloblastoma cells) and a murine pre-osteoblast cell line (MC3T3-E1 cells). We treated each cell type with the conditioned medium by the other cell type. We analyzed the effect on cytokine production by MC3T3-E1 cells and the production of MMPs by AM-3 cells. Treatment with AM-3-conditioned medium induced inflammatory cytokine production of IL-6, MCP-1, and RANTES from MC3T3-E1 cells. The use of an IL-1 receptor antagonist suppressed the production of these inflammatory cytokines by MC3T3-E1 cells stimulated with AM-3-conditioned medium. The MC3T3-E1-conditioned medium triggered the expression of MMP-2 from AM-3 cells. Furthermore, we have shown that the proliferation and migration activity of AM-3 cells were accelerated by MC3T3-E1 conditioned media. In conclusion, these intercellular signalings between ameloblastoma cells and osteoblasts may play multiple roles in the pathogenesis of ameloblastoma.

    DOI: 10.1016/j.bbrep.2022.101233

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  • Bakkalci D. .  Bioengineering the ameloblastoma tumour to study its effect on bone nodule formation .  Scientific Reports11 ( 1 ) 24088   2021.12

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    Language:Japanese   Publisher:Scientific Reports  

    Ameloblastoma is a benign, epithelial cancer of the jawbone, which causes bone resorption and disfigurement to patients affected. The interaction of ameloblastoma with its tumour stroma drives invasion and progression. We used stiff collagen matrices to engineer active bone forming stroma, to probe the interaction of ameloblastoma with its native tumour bone microenvironment. This bone-stroma was assessed by nano-CT, transmission electron microscopy (TEM), Raman spectroscopy and gene analysis. Furthermore, we investigated gene correlation between bone forming 3D bone stroma and ameloblastoma introduced 3D bone stroma. Ameloblastoma cells increased expression of MMP-2 and -9 and RANK temporally in 3D compared to 2D. Our 3D biomimetic model formed bone nodules of an average surface area of 0.1 mm2 and average height of 92.37 ± 7.96 μm over 21 days. We demonstrate a woven bone phenotype with distinct mineral and matrix components and increased expression of bone formation genes in our engineered bone. Introducing ameloblastoma to the bone stroma, completely inhibited bone formation, in a spatially specific manner. Multivariate gene analysis showed that ameloblastoma cells downregulate bone formation genes such as RUNX2. Through the development of a comprehensive bone stroma, we show that an ameloblastoma tumour mass prevents osteoblasts from forming new bone nodules and severely restricted the growth of existing bone nodules. We have identified potential pathways for this inhibition. More critically, we present novel findings on the interaction of stromal osteoblasts with ameloblastoma.

    DOI: 10.1038/s41598-021-03484-5

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  • Sarkar R. .  Effect of cigarette smoke extract on mitochondrial heme-metabolism: An in vitro model of oral cancer progression .  Toxicology in Vitro60   336 - 346   2019.10

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    Publisher:Toxicology in Vitro  

    DOI: 10.1016/j.tiv.2019.06.016

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  • Fuchigami T. .  Fibroblasts promote the collective invasion of ameloblastoma tumor cells in a 3D coculture model .  FEBS Open Bio7 ( 12 ) 2000 - 2007   2017.12

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    Publisher:FEBS Open Bio  

    DOI: 10.1002/2211-5463.12313

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  • Harada Takeshi, Yamamoto Hideki, Kishida Shosei, Kishida Michiko, Awada Chihiro, Takao Toshifumi, Kikuchi Akira .  Wnt5B関連エクソソームは癌細胞の遊走と増殖を促進する(Wnt5b-associated exosomes promote cancer cell migration and proliferation) .  Cancer Science108 ( 1 ) 42 - 52   2017.1Wnt5B関連エクソソームは癌細胞の遊走と増殖を促進する(Wnt5b-associated exosomes promote cancer cell migration and proliferation)

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    Publisher:John Wiley & Sons Australia, Ltd  

    癌進展におけるWnt5Bの役割を明らかにするため、Wnt5Bの生化学的特性と、癌細胞からのWnt5B分泌モードについて調べた。その結果、Wnt5Bは三つのアスパラギン残基がグリコシル化し、一つのセリン残基では脂質が付加されており、これらの翻訳後修飾がWnt5Bの分泌に不可欠であることが明らかになった。精製したWnt5BはDvl2リン酸化とRac活性化能においてWnt5aと同等であった。PANC-1膵癌細胞では、分泌されたWnt5Bの55%はエクソソームに関係していた。野生型PANC-1細胞のエクソソームはCHO細胞でWnt5Bシグナル系を活性化し、A549肺腺癌細胞の遊走と増殖を刺激した。これはエクソソーム関連Wnt5Bに活性があることを示唆していた。CHO細胞に取り込まれたエクソソームを免疫顕微鏡で調べた結果、Wnt5Bは確かにエクソソームに関連していた。Wnt5B関連エクソソームは膵癌において癌細胞の増殖と遊走を促進することが示唆された。

  • Macha M.A. .  Afatinib radiosensitizes head and neck squamous cell carcinoma cells by targeting cancer stem cells .  Oncotarget8 ( 13 ) 20961 - 20973   2017

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    Publisher:Oncotarget  

    DOI: 10.18632/oncotarget.15468

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  • FUCHIGAMI Takao., KOYAMA Hirofumi., KISHIDA Shosei., IIJIMA Mikio., NISHIZAWA Yoshiaki., HIJIOKA Hiroshi., FUJII Tomomi., UEDA Masahiro., NAKAMURA Norifumi., KIYONO Touru., KISHIDA Michiko. .  Regulation of IL-6 and IL-8 Production by Reciprocal Cell-to-CellInteractions between Tumor Cells and Stromal Fibroblasts through IL-1<alpha> inAmeloblastoma .  Biochemical and Biophysical Research Communications 451 ( 4 ) 491 - 496   2014.9Regulation of IL-6 and IL-8 Production by Reciprocal Cell-to-CellInteractions between Tumor Cells and Stromal Fibroblasts through IL-1<alpha> inAmeloblastomaReviewed

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    Language:English   Publishing type:Research paper (scientific journal)  

  • HABU Mika., KOYAMA Hirofumi., KISHIDA Michiko., KAMINO Masayuki., IIJIMA Mikio., FUCHIGAMI Takao., TOKIMURA Hiroshi., UEDA Masahiro., TOKUDOME Mai., KORIYAMA Chihaya., HIRANO Hirofumi., ARITA Kazunori. and KISHIDA Shosei. .  Ryk is essential for Wnt-5a-dependent invasiveness in human glioma. .  Journal of Biochemistry156 ( 1 ) 29 - 38   2014.7Ryk is essential for Wnt-5a-dependent invasiveness in human glioma.Reviewed

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  • KIBE Toshiro, FUCHIGAMI Takao, KISHIDA Michiko, IIJIMA Mikio, Ishihata K, HIJIOKA Hiroshi, MIYAWAKI A, SENBA Ichiro, NAKAMURA Norifumi, KIYONO Tohru, KISHIDA Srhosei. .  A novel ameloblastoma cell line (AM-3) secretes MMP-9 in response to Wnt-3a and induces osteoclastogenesis. .  Oral Surg Oral Med Oral Pathol Oral Radiol.115 ( 6 ) 780 - 788   2013.6A novel ameloblastoma cell line (AM-3) secretes MMP-9 in response to Wnt-3a and induces osteoclastogenesis.Reviewed

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  • HAYASHI Takehiro, KISHIDA Michiko, NISHIZAWA Yoshiaki, IIJIMA Mikio, KORIYAMA Chihaya, NAKAMURA Masayuki, SANA Akira, KISHIDA Shosei .  Subcellular localization and putative role of VPS13A/chorein in dopaminergic neuronal cells. .  Biochemical and Biophysical Research Communication, Elsevier419   511 - 516   2012.4Subcellular localization and putative role of VPS13A/chorein in dopaminergic neuronal cells.Reviewed

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  • KIBE Toshiro, KISHIDA Michiko, KAMINO Masayuki, IIJIMA Mikio, CHEN Lin, HABU Mika, MIYAWAKI Akihiko, HIJIOKA Hiroshi, NAKAMURA Norifumi, KIYONO Tohru, KISHIDA Shosei .  Immortalization and Characterization of Normal Oral Epithelial Cells without Using HPV and SV40 genes .  Oral Science International8 ( 1 ) 20 - 28   2011.4Immortalization and Characterization of Normal Oral Epithelial Cells without Using HPV and SV40 genesReviewed

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  • KAMINO Masayuki, KISHIDA Michiko, KIBE Toshiro, IKOMA Kyoko, IIJIMA Mikio, HIRANO Hirofumi, TOKUDOME Mai, CHEN Lin, KORIYAMA Chihaya, YAMADA Katsushi, ARITA Kazunori, KISHIDA Shosei .  Wnt-5a signaling is correlated with infiltrative activity in human glioma by inducing cellular migration and MMP-2 .  Cancer Science3 ( 3 ) 540 - 548   2011.3Wnt-5a signaling is correlated with infiltrative activity in human glioma by inducing cellular migration and MMP-2Reviewed

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