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Affiliation |
Graduate School of Medicine Doctorial Course in Medicine Oncoregulatory Medicine Department of Molecular Medicine and Biochemistry |
Kuriyama sei
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Research Interests 【 display / non-display 】
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Cancer Biology
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Developmental Biology
Graduating School 【 display / non-display 】
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1992.04-1996.03
Kwansei Gakuin University Faculty of Science Graduated
Graduate School 【 display / non-display 】
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1998.04-2001.03
Kwansei Gakuin University Graduate School, Division of Science Doctor's Course Accomplished credits for doctoral program
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1996.04-1998.03
Kwansei Gakuin University Graduate School, Division of Science Master's Course Completed
Studying abroad experiences 【 display / non-display 】
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2006.10-2009.07
University College London BBSRC postdoctoral fellow
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2005.10-2006.10
University College London Honorary Postdoctoral fellow
Campus Career 【 display / non-display 】
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2009.08-Now
Akita University Associate Professor
Research Areas 【 display / non-display 】
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Life Science / Tumor biology
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Life Science / Developmental biology
Research Achievements 【 display / non-display 】
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LPP inhibits collective cell migration during lung caner dissemination
Sei Kuriyama et al.
Oncogene 35 ( 8 ) 952 - 964 2016.06
Research paper (journal) Domestic Co-author
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In vivo collective cell migration requires an LPAR2-dependent increase in tissue fluidity.
Sei Kuriyama
Jornal Cell Biology ( 206 ) 113 - 127 2014.07 [Refereed]
Research paper (journal) Domestic Co-author
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Identification of anti-cancer chemical compounds using Xenopus embryos
Masamitsu Tanaka, Sei Kuriyama, Go Itoh, Aki Kohyama, Yoshiharu Iwabuchi, Hiroyuki Shibata, Masakazu Yashiro, Namiko Aiba
CANCER SCIENCE ( WILEY-BLACKWELL ) 107 ( 6 ) 803 - 811 2016.06 [Refereed]
Research paper (journal)
Cancer tissues have biological characteristics similar to those observed in embryos during development. Many types of cancer cells acquire pro-invasive ability through epithelial-mesenchymal transition (EMT). Similar processes (gastrulation and migration of cranial neural crest cells [CNCC]) are observed in the early stages of embryonic development in Xenopus during which cells that originate from epithelial sheets through EMT migrate to their final destinations. The present study examined Xenopus embryonic tissues to identify anti-cancer compounds that prevent cancer invasion. From the initial test of known anti-cancer drugs, AMD3100 (an inhibitor of CXCR4) and paclitaxel (a cytoskeletal drug targeting microtubules) effectively prevented migration during gastrulation or CNCC development. Blind-screening of 100 synthesized chemical compounds was performed, and nine candidates that inhibited migration of these embryonic tissues without embryonic lethality were selected. Of these, C-157 (an analog of podophyllotoxin) and D-572 (which is an indole alkaroid) prevented cancer cell invasion through disruption of interphase microtubules. In addition, these compounds affected progression of mitotic phase and induced apoptosis of SAS oral cancer cells. SAS tumors were reduced in size after intratumoral injection of C-157, and peritoneal dissemination of melanoma cells and intracranial invasion of glioma cells were inhibited by C-157 and D-572. When the other analogues of these chemicals were compared, those with subtle effect on embryos were not tumor suppressive. These results suggest that a novel chemical-screening approach based on Xenopus embryos is an effective method for isolating anti-cancer drugs and, in particular, targeting cancer cell invasion and proliferation.
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LPP inhibits collective cell migration during lung cancer dissemination
S. Kuriyama, M. Yoshida, S. Yano, N. Aiba, T. Kohno, Y. Minamiya, A. Goto, M. Tanaka
ONCOGENE ( NATURE PUBLISHING GROUP ) 35 ( 8 ) 952 - 964 2016.02 [Refereed]
Research paper (journal)
Lipoma preferred partner (LPP) is a LIM domain protein, which has multiple functions as an actin-binding protein and a transcriptional coactivator, and it has been suggested that LPP has some roles in cell migration or invasion, however, its role in cancer cells remains to be elucidated. Here, we showed that LPP degraded N-cadherin in lung cancer, PC14PE6 cells via regulating the expression of matrix metalloproteinase 15 (MMP-15), and loss-of-LPP increases collective cell migration (CCM) and dissemination consequently. Knockdown of LPP and its functional partner, Etv5, markedly restores the full-length N-cadherin and increases cell-cell adhesion. We investigated the common target of LPP and Etv5, and found that MMP-15 is transcribed as their direct transcriptional target. Furthermore, MMP-15 could directly digest the N-cadherin extracellular domain. LPP knockdown in PC14PE6 cells increases N-cadherin-dependent CCM in the three-dimensional collagen gel invasion assays, and promoted the dissemination of cancer cells when they were orthotopically implanted in nude mice. Immunohistochemistry of lung adenocarcinoma specimens revealed the heterogeneity of LPP intensity and complementary expression of LPP and N-cadherin in the primary tumors. These findings suggest that loss-of-LPP, Etv5 or MMP-15 can be a prognostic marker of increasing malignancy.
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Masamitsu Tanaka, Shintaro Shimamura, Sei Kuriyama, Daichi Maeda, Akiteru Goto, Namiko Aiba
CANCER RESEARCH ( AMER ASSOC CANCER RESEARCH ) 76 ( 2 ) 358 - 369 2016.01 [Refereed]
Research paper (journal)
Tumor-associated macrophages (TAM) play complex and pivotal roles during cancer progression. A subset of metastasis-associated macrophages accumulates within metastatic sites to promote the invasion and growth of tumor cells. Src kinase-associated phosphoprotein 2 (SKAP2), a substrate of Src family kinases, is highly expressed in macrophages from various tumors, but its contribution to the tumor-promoting behavior of TAMs is unknown. Here, we report that SKAP2 regulates podosome formation in macrophages to promote tumor invasion and metastasis. SKAP2 physically interacted with Wiskott-Aldrich syndrome protein (WASP) and localized to podosomes, which were rarely observed in SKAP2-null macrophages. The invasion of peritoneal macrophages derived from SKAP2-null mice was significantly reduced compared with wild-type macrophages, but could be rescued by the restoration of functional SKAP2 containing an intact tyrosine phosphorylation site and the ability to interact with WASP. Furthermore, SKAP2-null mice inoculated with lung cancer cells exhibited markedly decreased lung metastases characterized by reduced macrophage infiltration compared with wild-type mice. Moreover, intravenously injected SKAP2-null macrophages failed to efficiently infiltrate established tumors and promote their growth. Taken together, these findings reveal a novel mechanism by which macrophages assemble the appropriate motile machinery to infiltrate tumors and promote disease progression, and implicate SKAP2 as an attractive candidate for therapeutically targeting TAMs. (C) 2015 AACR.
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Kuriyama S, Tsuji T, Sakuma T, Yamamoto T, Tanaka M
Cell death discovery 4 ( 1 ) 11 2018.12
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Curcumin analog, GO-Y078, overcomes resistance to tumor angiogenesis inhibitors.
Shimazu K, Inoue M, Sugiyama S, Fukuda K, Yoshida T, Taguchi D, Uehara Y, Kuriyama S, Tanaka M, Miura M, Nanjyo H, Iwabuchi Y, Shibata H
Cancer science 109 ( 10 ) 3285 - 3293 2018.10
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Author Correction: Lateral attachment of kinetochores to microtubules is enriched in prometaphase rosette and facilitates chromosome alignment and bi-orientation establishment.
Itoh G, Ikeda M, Iemura K, Amin MA, Kuriyama S, Tanaka M, Mizuno N, Osakada H, Haraguchi T, Tanaka K
Scientific reports 8 ( 1 ) 7003 2018.04
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LPP阻害による肺がん細胞の集団化は浸潤を促進する
栗山 正, 吉田 誠, 矢野 聖二, 相場 なみ子, 河野 隆志, 南谷 佳弘, 後藤 明輝, 田中 正光
日本癌学会総会記事 ( 日本癌学会 ) 74回 E - 1138 2015.10
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LPPは肺がんの転移における集団的細胞移動を阻害する(LPP inhibits collective cell migration during lung cancer metastasis)
栗山 正, 矢野 聖二, 後藤 明輝, 田中 正光
日本癌学会総会記事 ( 日本癌学会 ) 73回 E - 2087 2014.09
◆Original paper【 display / non-display 】
◆Other【 display / non-display 】
Grant-in-Aid for Scientific Research 【 display / non-display 】
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Grant-in-Aid for Scientific Research(C)
Project Year： 2015.04 - 2018.03
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Grant-in-Aid for Young Scientists(B)
Project Year： 2012.04 - 2014.03