检查点基因CHFR在口腔鳞状细胞癌诊断和治疗中的应用。-猫眼课题宝

检查点基因CHFR在口腔鳞状细胞癌诊断和治疗中的应用。

批准号：

16390597

负责人：

TOKINO Takashi

金额：

$8.9万

依托单位：

Sapporo Medical 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

项目状态：

已结题

起止时间：

2004 至 2005

来源：

https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16390597/

关键词：

Cancer Translational Research Chemosensitivity Cell Cycle Control Ubiquitin ligase ユビキチンリガーゼ癌細胞周期有糸分裂チェックポイント微小管脱重合阻害剤口腔癌感受性診断

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中文摘要

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英文摘要

Alterations in the function of cell cycle checkpoints are frequently detected in oral squamous cell carcinomas (OSCCs), and are often associated with the sensitivity of the cancer cells to chemotherapeutic drugs. Recently, a mitotic checkpoint gene, Chfr, was shown to be inactivated by promoter methylation and point mutations in various human tumors. Here we show that the absence of its product, CHFR, is associated with mitotic checkpoint dysfunction, and that cancer cells lacking CHFR are sensitive to microtubule inhibitors. Checkpoint impairment appears to be caused by a prophase defect in this case, as OSCC cells lacking CHFR showed phosphorylation of histone H3 on Ser10 and translocation of cyclin B1 to the nucleus. When CHFR-deficient OSCC cells were treated with a microtubule inhibitor (docetaxel or paclitaxel), significant numbers of apoptotic cells were observed. Moreover, disruption of CHFR using small interfering RNA (siRNA) impaired the mitotic checkpoint, thereby reducing the ability of OSCC cells to arrest at G2/M phase and making them more sensitive to microtubule inhibitors. Our results suggest that CHFR could be a useful molecular target for chemotherapy.

期刊论文(70)

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科研奖励(0)

会议论文

Genetic, epigenetic and clinicopathological features of gastric cancers with CpG island methylator phenotype and association to Epstein-Barr virus.

具有 CpG 岛甲基化表型以及与 Epstein-Barr 病毒相关的胃癌的遗传、表观遗传和临床病理学特征。

DOI： --

发表时间： 2006

期刊：

C a n c e r 106(7)

影响因子： --

作者：

[Kusano M, Toyota M, Suzuki H, Akino K, Aoki F, Fujita M, Hosokawa M, Shinomura Y, Imai K, Tokino T]

通讯作者： Tokino T

Aberrant laminin beta3 isoforms downstream of EWS-ETS fusion genes in Ewing family tumors

尤文家族肿瘤中 EWS-ETS 融合基因下游的异常层粘连蛋白 beta3 亚型

DOI： --

发表时间： 2005

期刊：

Cancer Cell Ther 4

影响因子： --

作者：

[Irifune H, Nishimori H, Watanabe G, Yoshida K, Ikeda T, Matsui C, Morohashi M, Kawaguchi S, et al.]

通讯作者： et al.

Regulation of MHC class II expression in glioma cells by class II transactivator (CIITA)

DOI： 10.1002/glia.10343

发表时间： 2004-03-15

期刊：

GLIA

影响因子： 6.2

作者：

[Takamura, Y, Ikeda, H, Sato, N]

通讯作者： Sato, N

Tight junction protein MAGI-1 is up-regulated by transfection with connexin 32 in an immortalized mouse hepatic cell line : cDNA micrroarray analysis.

在永生化小鼠肝细胞系中，通过连接蛋白 32 转染，紧密连接蛋白 MAGI-1 上调：cDNA 微阵列分析。

DOI： --

发表时间： 2005

期刊：

Cell Tissue Research 319・2

影响因子： --

作者：

[N.Saitoh, et al., Irifune H et al., Odajima T et al., Murata M et al.]

通讯作者： Murata M et al.

Epigenetic inactivation of classII transactivator (CIITA) is associated with the absence of interferon-gamma-induced HLA-DR expression in colorectal and gastric cancer cells.

II 类反式激活因子 (CIITA) 的表观遗传失活与结直肠癌细胞和胃癌细胞中干扰素 γ 诱导的 HLA-DR 表达缺失有关。

DOI： --

发表时间： 2004

期刊：

Oncogene 23・55

影响因子： --

作者：

[Nakano K, Nomura R, Shimizu N, Nakagawa I, Hamada S, Ooshima T., Nakano K et al., Maruyama R et al., Akino K et al., Kang X et al., Kusano M et al., King KE et al., Okuda H et al., Terasawa K et al., Maruyama R et al., Akino K et al., Kang X et al., Kusano M et al., King KE et al., Okuda H et al., Terasawa K et al., Maruyama et al., Kusano M et al., King KE et al., Terasawa K et al., Kang X et al., Ogi K et al., Sasaki Y et al., Irifune H et al., Aoki M et al., Simbulan-Rosenthal CM et al., Murai M et al., Ikeda H et al., Murai M et al., Odajima T et al., Murata M et al., Abe T et al., Ogi K et al., Sasaki Y et al., Irifune H et al., Aoki M et al., Simbulan-Rosenthal CM et al., Murai M et al., Ikeda H et al., Murai M et al., Odajima T et al., Murata M et al., Abe T et al., Ogi K et al., Odajima T et al., Abe T et al., Aoki M, Murata M, Adachi K et al., Suzuki H et al., Tokino T, Satoh A et al.]

通讯作者： Satoh A et al.