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World Science Leader’s Seminar (WSLS)

2015/11/20

2015年11月20日(金)に筑波大学「ヒューマンバイオロジー学位プログラム」が主催となり,World Science Leader’s Seminarを開催いたします。World Science Leader’s Seminarは、サイエンスの世界で活躍されている方々にお越しいただき,トップレベルの知識と技術をご指導いただく貴重な機会です。今回の講演者は,Dr. Aristidis Moustakas(Professor, Dept. of Medical Biochemistry and Microbiology, Uppsala University)です。どなたでも参加可能ですので,ふるってご参加ください。尚,本セミナーは英語で行われます。

開催日時:2015年11月20日(金)17:00~18:30

会 場 :総合研究棟D115GooglrMap版へ
アクセス:
筑波大学筑波キャンパスへは「筑波キャンパスへの交通アクセス」をご覧ください。
利用停留所(関東鉄道バス):筑波大学中央行き又は筑波大学循環バス「平砂学生宿舎前

ゲストスピーカー:Dr. Aristidis Moustakas (Professor, Dept. of Medical Biochemistry and Microbiology, Uppsala University)

セミナータイトル:Plasticity in tumor cell differentiation

アブストラクト:
Epithelial-mesenchymal transition (EMT) contributes to tumor cell invasiveness and the generation of cancer stem cells. Our laboratory aims at deciphering molecular mechanisms that link EMT to the generation and maintenance of cancer stem cells. We study the nuclear protein high mobility group A2 (HMGA2) that is required for the induction of EMT by transforming growth factor β (TGFβ) (Thuault et al. J. Cell Biol. 174:175-83, 2006). HMGA2 regulates a cohort of transcriptional regulators of the EMT process, such as Snail1 and Twist1 (Thuault et al. J. Biol. Chem. 283:33437-46, 2008; Tan et al. J. Biol. Chem. 287:7134-45). HMGA2 is an embryonic chromatin factor that is gradually and steadily downregulated during adult life with the exception of tissue stem cells, where its downregulation is induced by the aging process. Signal transduction by TGFβ and its related polypeptides, bone morphogenetic proteins (BMPs), coordinates physiological responses in diverse cell types. TGFβ promotes EMT, tumor cell invasiveness and metastasis, while BMP promotes mesenchymal-epithelial transition (MET) and suppresses tumorigenicity. The work that we will present focuses on the role of HMGA2 in breast carcinoma cell invasion and stem cell survival. Breast cancer cells that express high or lower levels of HMGA2 present a corresponding degree of self-renewal based on mammosphere assays. When HMGA2 is silenced from aggressive breast cancer cells, the phenotype shifts to an epithelial, indicative of MET, and concomitantly, tumor cells lose their self-renewing capacity. Transcriptomic analysis identified genes that are regulated by HMGA2 and which functionally link to the processing of miRNA biogenesis. Finally, by focusing on non-epithelial cancer stem cells, namely glioblastoma, we demonstrate that the ability of BMP to suppress glioma cancer stem cell self-renewal and tumorigenic potential depends on the transcriptional induction of Snail1, which induces differentiation of glioma cells and promotes a dramatic invasion of these cells within the recipient brain, while depleting the tumorigenicity from the same cells. Our work starts explaining in molecular detail how embryonic nuclear factors like HMGA2 and Snail1, when reactivated in human cancer, provide coordinated control of multiple genes, thus, promoting both the mesenchymal transition and tumor cell invasiveness, while, depending on the cell type of origin, they either promote or suppress cancer stem cell self-renewal.

主催:筑波大学 ヒューマンバイオロジー学位プログラム

連絡先
住所 〒305-8577 茨城県つくば市天王台1-1-1
総合研究棟A グローバル教育院事務室
Mail sigma#@#un.tsukuba.ac.jp(#@#を 「@」 に置き換えてください)
TEL 029-853-7085

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