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

本研究的目的之一是实现“我们确定由于癌细胞的细胞粘附机制而产生的辐射抗性因子，并靶向分子和信号转导的辐射敏感增敏”。我们参与了去年继发的癌细胞的细胞浸润和转移的控制，并主要对Dyasdherin进行了研究，Dyasdherin是一种粘附因子，它将E-钙粘蛋白的功能控制为负数，并与放射线敏感性相关，今年获得了以下结果。利用不同辐射敏感性的人癌细胞培养细胞，检测了Dyasdherin的表现和细胞增殖能力以及体外辐射敏感性。结果，如果Dyasdherin的表现高，则假定生长标记物为指标的增殖能力高，并且放射线敏感性倾向于低。表现为辐射后增强改变，无明显的放射性损伤。 ...更多信息 当我们检查2）照射引起的Dyasdherin表现的变化时，随着这些表现的改变，我们证实了信号的激活与EGFR协同作用并被激活。这些结果是继续研究的地方，现在更多的是确定机制和相关的信号通路，这表明细胞粘附因子与癌细胞的辐射应答相关的可能性。特别地，我们关注我们平行检测的细胞生长因子受体与癌细胞的辐射应答的关系。EGFR和HER 2的激活和局部变化（从细胞表面到细胞核）是由辐射诱导的，但是当我们抑制激活时，局部变化被修饰。结果，我们确认我们抑制了辐射引起的DNA损伤修复过程，并参与了辐射敏感性变化（辐射敏感性增强）。我们研究了这些信号转导的激活和细胞死亡的介体，并且主要基于与信号的串扰的存活，这是由于细胞粘附因子。分子和信号转导工作主要通过这种分析发现并确认它如何辐射反应的癌细胞的变化通过激活抑制和表现抑制，我们检查的可能性作为治疗目标，并将报告它。减

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