The radiobiological study of radio-sensitization targeting molecules and/or signal transduction pathways that are involved in cell adhesion.

对参与细胞粘附的放射增敏靶向分子和/或信号转导途径的放射生物学研究。

基本信息

批准号：
21591620
负责人：
AKIMOTO Tetsuo
金额：
$ 2.83万
依托单位：
独立行政法人国立がん研究センター (2011)Tokyo Women's Medical University (2009-2010)
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2009
资助国家：
日本
起止时间：
2009 至 2011
项目状态：
已结题

项目摘要

A purpose of this study is to achieve "the radiosensitive sensibilization that we determine a radioresistant factor due to the cell adhesion mechanism of the cancer cell, and targeted the molecules and signal transduction". We are involved in the control of cellular infiltration and the metastasis of the cancer cell secondary to last year and examine it mainly on Dyasdherin which is an adhesion factor providing it controlling a function of E-cadherin to minus number and a correlation with the radiation sensitivity and obtain the following results this year. Using the human cancer cell cultured cell which varied in radiation sensitivity, we examined manifestation of Dyasdherin and cellular proliferative capacity and radiation sensitivity in vitro. As a result, the proliferation potency that assumed a growth marker an index if manifestation of Dyasdherin is high is high, and radiation sensitivity tend to be low. The manifestation enhance the change after the radiation that there is not o … More f the things in the localization temporarily when we examine a change of the Dyasdherin manifestation with 2) irradiation. With a change of these 3) manifestation, we confirm that the activation of the signal acts in concert with EGFR and is activated. These results are places continuing a study more now to determine the mechanism and associated signaling pathway with a thing suggesting the possibility that a cell adhesion factor is associated with the radiation reply of the cancer cell. Particularly, we pay attention to the relations with the radiation reply of a cell growth factor receptor and the cancer cell which we are parallel and examine. Activation of EGFR and HER2 and the localized change(from the cell surface to a nucleus) are induced by irradiation, but the localized change is adorned when we inhibit the activation. As a result, we confirm that we inhibit a DNA lesion repairing process by the radiation and are involved in a radiosensitive change(radiosensitive augmentation). We examined a mediator about activation and cell death of these signal transduction and the survival mainly on the crosstalk with the signal which was due to a cell adhesion factor. Molecules and signal transduction working primary by this analysis find and confirm it how the radiation reply of the cancer cell changes by the activation inhibition and manifestation suppression and we examine the likelihood as the treatment target and are going to report it. Less

这是“我们确定癌细胞的放射线，并针对分子和信号转导的目的”。它主要是控制它控制umber的粘附力，并与辐射灵敏度的相关性，并获得以下结果，今年的细胞培养细胞在辐射敏感性方面有所不同。生长标记是指dyasdherin的表现高，并且辐射离子敏感性增强了辐射的辐射，当韦克萨明的定位临时车轮是dyasdherin的表现，并带有2）辐照。信号与EGFR一起起作用。对于细胞grof因子因子的辐射和癌细胞的辐射，我们是平行的并检查了EGFR和HER2的激活。辐射的激活过程，并参与辐射式（辐射式）。通过此分析进行主要工作，发现并确认了癌细胞的辐射。