To explore miR-195 mechanisms of acquired resistance against TMZ in glioblastoma.

探讨胶质母细胞瘤中 miR-195 对 TMZ 获得性耐药的机制。

• 批准号: 23592095
• 负责人: UJIFUKU Kenta
• 金额: $ 3.33万
• 依托单位: Nagasaki University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23592095/
• 关键词: 脳腫瘍; 神経膠芽腫; 脳血管関門; FGF-2; Niche; 脳血管関門モデル; 悪性腫瘍; 核酸; 組織細胞; 脳神経疾患; マイクロRNA; マイクロＲＮＡ

The initial purpose of this study was to explore miR-195 mechanisms of acquired resistance against TMZ in glioblastoma (GBM). Unexpected results have been obtained and they have not been published yet.Alternative study approach has been performed and intriguing results have been obtained. This study was examined to explore the mechanism of invasion front niche of GBM. Using new in vitro blood brain barrier (BBB) models, interaction between BBB and GBM was explored. In acute phase of the interaction, GBM could strengthen BBB, and FGF-2 might be implicated in the process. These results have been published.

本研究的初步目的是探讨胶质母细胞瘤(GBM)对TMZ获得性耐药的miR-195机制。已经获得了意想不到的结果，但尚未发表。另一种研究方法已经进行，并获得了耐人寻味的结果。本研究旨在探讨GBM入侵前部生态位的机制。采用新的体外血脑屏障(BBB)模型，探讨血脑屏障与GBM之间的相互作用。在相互作用的急性期，GBM可增强血脑屏障，可能与成纤维细胞生长因子-2有关。这些成果已经发表。

项目成果

MiRNA-205 modulates cellular invasion and migration via regulating zinc finger E-box binding homeobox 2 expression in esophageal squamous cell carcinoma cells.

• DOI: 10.1186/1479-5876-9-30
• 发表时间: 2011-03-22
• 期刊: Journal of translational medicine
• 影响因子: 7.4
• 作者: Matsushima K;Isomoto H;Yamaguchi N;Inoue N;Machida H;Nakayama T;Hayashi T;Kunizaki M;Hidaka S;Nagayasu T;Nakashima M;Ujifuku K;Mitsutake N;Ohtsuru A;Yamashita S;Korpal M;Kang Y;Gregory PA;Goodall GJ;Kohno S;Nakao K
• 通讯作者: Nakao K