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

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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