Invasiveness acquired during EMT

EMT 期间获得的侵袭性

• 批准号: 20247027
• 负责人: SABE Hisataka
• 金额: $ 20.63万
• 依托单位: Hokkaido University (2009-2011)Osaka Bioscience Institute (2008)
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (A)
• 财政年份: 2008
• 资助国家: 日本
• 起止时间: 2008 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-20247027/
• 关键词: EMT; 浸潤; Arf GTPases; E-cadherin; endocytosis; AMAP1; TGFβ1; p53; 細胞浸潤; Arf6; GEP100

This study aims to understand precise mechanisms by which epithelial cells acquire invasiveness during their epithelial-mesenchymal transdifferentiation (EMT). Inactivation of E-cadherin and activation of some integrins are hallmark characteristics during EMT and necessary for the invasiveness. This study identified fine mechanisms as to how these cell adhesion molecules are regulated during EMT of mammary epithelial cells.

本研究旨在了解上皮细胞在上皮-间充质转分化（EMT）过程中获得侵袭性的确切机制。e -钙粘蛋白的失活和一些整合素的激活是EMT的标志性特征，也是侵袭性的必要条件。本研究确定了乳腺上皮细胞EMT过程中这些细胞粘附分子调控的精细机制。

项目成果

Mutant p53 is essential for TGFβ1-induced breast cancer cell invasion

突变的p53对于TGFβ1诱导的乳腺癌细胞侵袭至关重要

• 发表时间: 2011
• 作者: Nozaki;H.;Coleman;A.W.;橋本あり
• 通讯作者: 橋本あり

p53 mutation and TGFβ signaling culminate in cancer invasiveness via GEP100-Arf6-AMAP1 pathway

p53 突变和 TGFβ 信号传导通过 GEP100-Arf6-AMAP1 途径最终导致癌症侵袭

• 发表时间: 2011
• 作者: Morishige M.;Hashimoto S.;Ogawa E.;Toda Y.;Kotani H.;Hirose M.;Wei S.;Hashimoto A.;Yamada A.;Yano H.;Mazaki Y.;Kodama H.;Nio Y.;Manabe T.;Wada H.;Kobayashi H.;Sabe H.;小林昇平;佐邊壽孝
• 通讯作者: 佐邊壽孝

Glucose metabolism and intracellular trafficking in tumor malignancy

肿瘤恶性肿瘤中的葡萄糖代谢和细胞内运输

• 发表时间: 2011
• 作者: H. Asakawa;Y. Hiraoka;小野寺康仁
• 通讯作者: 小野寺康仁

EPB41L5 functions to post-transcriptionally regulate cadherin and integrin during pithelial-mesenchymal transition.

EPB41L5 在上皮-间质转化过程中发挥转录后调节钙粘蛋白和整合素的作用。

• 发表时间: 2008
• 期刊: J Cell Biol. 182
• 作者: Hirano M.;Hashimoto S.;Yonemura S.;Sabe H.;Aizawa S.
• 通讯作者: Aizawa S.

Mutant p53 is essential for TGFβ1-induced breast cancer cellinvasion

突变的p53对于TGFβ1诱导的乳腺癌细胞侵袭至关重要

• 发表时间: 2011
• 作者: Yang;Y.;Maruyama;S.;Sekimoto;H.,Sakayama;H. & Nozaki;H;橋本あり
• 通讯作者: 橋本あり