Analysis of human synovial sarcoma oncoprotein SYT-SSX and its therapeutic application.

人滑膜肉瘤癌蛋白SYT-SSX的分析及其治疗应用。

• 批准号: 16390426
• 负责人: TANAKA Shinya
• 金额: $ 7.17万
• 依托单位: Hokkaido University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B)
• 财政年份: 2004
• 资助国家: 日本
• 起止时间: 2004 至 2006
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16390426/
• 关键词: SYT-SSX; synovial sarcoma; Brm; p21; choromatin remodeling; sarcoma; orthonedic surgery; 滑膜肉腫; クロマチン変換; 細胞老化; シグナル伝達; 軟部腫瘍; senescence; p21WAF1; トランスジェニックマウス

The cause of synovial sarcoma had been unknown for long time, and in 1994, Clark et al., identify the chimeric gene of t(X;18) and named it SYT-SSX. Then molecular analysis of SYT-SSX has been advanced and we have shown that SYT-SSX serves oncogenic potential on cells (Nagai, M., et al., PNAS, 2001).In this project, SYT-SSX was found to bind to not only one of the chromatin remodeling factors, hBRM, but to BRG (Gene Cells, 9, 2004), and also shown to induce cellular senescence by the induction of p21 (Oncogene, 24, 2005). Furthermore, IGF2 has been shown to play an important role for growth of synovial sarcoma cells (Oncogene, 25, 2006). We have shown that signaling adaptor protein Crk is indispensable for tumorigenesity of synovial sarcoma cell lines (Mol. Cancer Res., 7, 2006).One of the purpose of this project is to obtain the possible target molecules for synovial sarcoma treatment. As Crk knockdown cells is not going to die, but the malignant features were eliminated, thus, Crk may be the therapeutic target for the treatment of this sarcoma, and we will continue to analyze the mechanism of Crk for malignant character of synovial sarcoma.

滑膜肉瘤的病因长期不明，1994年，Clark等，鉴定了t（X;18）的嵌合基因，命名为SYT-SSX。然后，SYT-SSX的分子分析已经进展，并且我们已经表明SYT-SSX对细胞具有致癌潜力（永井，M.，例如，在该项目中，发现SYT-SSX不仅与染色质重塑因子之一hBRM结合，而且与BRG结合（Gene Cells，9，2004），并且还显示通过诱导p21诱导细胞衰老（Oncogene，24，2005）。此外，IGF 2已显示对滑膜肉瘤细胞的生长起重要作用（Oncogene，25，2006）。我们已经表明，信号转导衔接蛋白Crk是滑膜肉瘤细胞系的致瘤性不可或缺的（Mol.癌症研究所，7，2006）。本项目的目的之一是获得滑膜肉瘤治疗的可能靶分子。由于Crk基因敲低后细胞不会死亡，但恶性特征被消除，因此Crk可能成为治疗该肉瘤的治疗靶点，我们将继续分析Crk对滑膜肉瘤恶性特征的作用机制。

项目成果

Biomechanical study on the effect of five different lumbar reconstruction techniques on adjacent-level intradiscal pressure and lamina strain

• DOI: 10.3171/spi.2006.5.2.150
• 发表时间: 2006-08-01
• 期刊: JOURNAL OF NEUROSURGERY-SPINE
• 影响因子: 2.8
• 作者: Sudo, Hideki;Oda, Itaru;Minami, Akio
• 通讯作者: Minami, Akio

Azathioprine suppresses ERM-dependent T cell-APC conjugation through inhibition of Vav guanosine exchange activity on Rac proteins.

硫唑嘌呤通过抑制 Rac 蛋白上的 Vav 鸟苷交换活性来抑制 ERM 依赖性 T 细胞-APC 接合。

• 发表时间: 2006
• 期刊: J. Immunol. 176
• 作者: Poppe;D.
• 通讯作者: D.

Characterization and application of polyclonal antibodies that specifically recognize JC virus large T antigen.

特异性识别JC病毒大T抗原的多克隆抗体的表征及应用。

• 发表时间: 2006
• 期刊: Acta Neuropathol. (Berl) 111
• 作者: Sunden;Y.
• 通讯作者: Y.

A LONG-TERM FOLLOW-UP OF SILICONE-RUBBER INTERPOSITION ARTHROPLASTY FOR OSTEOARTHRITIS OF THE THUMB CARPOMETACARPAL JOINT

• DOI: 10.1142/s0218810405002607
• 发表时间: 2005-07-01
• 期刊: JOURNAL OF HAND SURGERY-ASIAN-PACIFIC VOLUME
• 影响因子: 0.5
• 作者: Minami, Akio;Iwasaki, Norimasa;Yasuda, Kazunori
• 通讯作者: Yasuda, Kazunori

The effect of transforming growth factor-beta on mechanical properties of the fibrous tissue regenerated in the patellar tendon after resecting the central portion

• DOI: 10.1016/j.clinbiomech.2005.05.012
• 发表时间: 2005-11-01
• 期刊: CLINICAL BIOMECHANICS
• 影响因子: 1.8
• 作者: Anaguchi, Y;Yasuda, K;Hayashi, K
• 通讯作者: Hayashi, K