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所属 |
大学院医学系研究科（医学専攻等） 医学専攻 腫瘍制御医学系 分子生化学講座 |
出身大学院 【 表示 ／ 非表示 】
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1998年04月-2001年03月
関西学院大学 理学系研究科 化学専攻 博士課程 単位取得満期退学
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1996年04月-1998年03月
関西学院大学 理学系研究科 化学専攻 修士課程 修了
留学履歴 【 表示 ／ 非表示 】
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2006年10月-2009年07月
ロンドン大学(UCL) BBSRCポストドクトラルフェロー
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2005年10月-2006年10月
ロンドン大学 上原記念生命科学財団海外留学フェロー
研究等業績 【 表示 ／ 非表示 】
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LPP inhibits collective cell migration during lung caner dissemination
Sei Kuriyama et al.
Oncogene 35 ( 8 ) 952 - 964 2016年06月
研究論文（学術雑誌） 国内共著
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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年07月 [査読有り]
研究論文（学術雑誌） 国内共著
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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年06月 [査読有り]
研究論文（学術雑誌）
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年02月 [査読有り]
研究論文（学術雑誌）
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年01月 [査読有り]
研究論文（学術雑誌）
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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Characteristic tetraspanin expression patterns mark various tissues during Xenopus early development.
Sei Kuriyama, Masamitsu Tanaka
Development, growth & differentiation 2023年01月
Tetraspanins (Tspans) are a four-pass transmembrane domain cell surface protein family. Tspans have been found on the plasma membrane and exosomes of various organelles. Reports on the function of tetraspanins during the early development of Xenopus have mainly focused on the expression of uroplakins in gametes. Although the roles of extracellular vesicles (EVs) including exosomes have been actively analyzed in cancer research, the contribution of EVs to early development is not well understood. This is because the diffusible property of EVs is not compatible with a very strict developmental process. In this study, we analyzed members of the tetraspanins in early development of Xenopus. The expression pattern was prominent in specific organs such as the notochord, eye, cranial neural crest cells (CNCs), trunk neural crest cells, placodes, and somites. We tested overexpressions of several different combination of Tspans expressing in CNC in vitro, and in vivo. Changing the partner changed the distribution of fluorescent-labeled Tspans. Therefore, it suggested that multiple Tspan expressions in particular tissue might produce heterogeneity of intercellular communication, which has not yet been recognized.
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CCDC85AはmiR-224により発現制御され、癌細胞の小胞体ストレス抵抗性に寄与する(Exosomes-mediated transfer of hsa-miR-224-3p augments ER-stress in cancer cells via targeting CCDC85A)
田中 正光, 高橋 壮, 高金 くらら, 伊藤 剛, 栗山 正, 後藤 明輝
日本癌学会総会記事 ( (一社)日本癌学会 ) 81回 P - 3080 2022年09月
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Kuriyama S.
Frontiers in Oncology ( Frontiers in Oncology ) 12 2022年01月
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研究者の最新動向 線維芽細胞による腫瘍進展システム
伊藤 剛, 高金 くらら, 福士 由真, 栗山 正, 田中 正光
Precision Medicine ( (株)北隆館 ) 4 ( 14 ) 1347 - 1350 2022年01月
間質細胞はがん細胞に刺激されるとがん進展を促進する細胞へと変化してしまう。例えば、この刺激により間質線維芽細胞はCAF(Cancer Associated Fibroblast)へと変化し、組織深部へのがん浸潤の促進効果を生み出している。これまでがん細胞-間質細胞の応答は注目されてきたが、CAF-間質細胞の応答はがん研究における新たな着眼であった。本稿では所属研究室(田中正光教授)で報告したCAF-正常な間質線維芽細胞の応答がいかにがん進展へと関与するかを紹介していく。(著者抄録)
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SKAP2 suppresses inflammation-mediated tumorigenesis by regulating SHP-1 and SHP-2
Takagane K.
Oncogene ( Oncogene ) 2022年
◆原著論文【 表示 ／ 非表示 】
◆その他【 表示 ／ 非表示 】
科研費（文科省・学振）獲得実績 【 表示 ／ 非表示 】
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がん遠隔転移における集団的細胞遊走の優位性の検証
基盤研究(C)
研究期間: 2015年04月 - 2018年03月
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細胞接触センサーから直接伝わる細胞骨格編集シグナルの研究
新学術領域研究
研究期間: 2013年04月 - 2015年03月
アフリカツメガエルの神経堤細胞を用いた細胞移動の研究において、我々は集団を維持するための細胞接着と移動を促進するための上皮間充織遷移(EMT)がどのようなバランスで行われているかについて調べた。
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細胞接着の安定化を用いたヒトがん細胞の直接浸潤抑制の研究
若手研究(B)
研究期間: 2012年04月 - 2014年03月