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

本研究的一个目的是实现辐射增敏，即我们根据癌细胞的细胞黏附机制，确定一种辐射抵抗因子，并针对分子和信号转导。我们去年参与了对癌细胞的侵袭和转移的控制，主要是对Dyasdherin的研究，Dyasdherin是一种黏附因子，它提供了一种控制E-cadherin功能的负数以及与辐射敏感性的相关性，并在今年获得了以下结果。利用辐射敏感性不同的人癌细胞培养细胞，检测Dyasdherin在体外的表现及细胞增殖能力和辐射敏感性。因此，如果Dyasdherin的表现较高，则假设生长标记为指标的增殖潜力较高，而辐射敏感性往往较低。辐射后无…的表现增强变化当我们观察照射后Dyasdherin表现的变化时，更多的是暂时定位的东西。随着这些表现的改变，我们确认信号的激活与EGFR协同作用并被激活。这些结果是现在继续进行更多研究的地方，以确定机制和相关的信号通路，表明细胞黏附因子与癌细胞的辐射应答有关的可能性。特别是我们平行检测的癌细胞与细胞生长因子受体的辐射应答的关系。辐射可以诱导EGFR和HER2的激活和局部变化(从细胞表面到细胞核)，但当我们抑制这种激活时，这种局部变化被修饰。因此，我们证实，我们抑制了辐射对DNA损伤的修复过程，并参与了辐射敏感性的变化(辐射敏感性增强)。我们检测了一种关于这些信号转导的激活和细胞死亡的介体，而存活主要取决于与信号的串扰，这是由于一种细胞黏附因子所致。通过这种分析，初步发现并证实了癌细胞的辐射应答是如何通过激活、抑制和表现抑制而发生变化的，并考察了其作为治疗靶点的可能性并予以报道。较少

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