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Repeated X-RAY Irradiation Generates the Radioresistant Cancer Cell that Underwent Epithelial to Mesenchymal Transition
https://repo.qst.go.jp/records/65224
https://repo.qst.go.jp/records/65224092f10dd-1ec9-4c52-9a54-f9e289e08b7b
| Item type | 会議発表用資料 / Presentation(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2013-10-24 | |||||
| タイトル | ||||||
| タイトル | Repeated X-RAY Irradiation Generates the Radioresistant Cancer Cell that Underwent Epithelial to Mesenchymal Transition | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_c94f | |||||
| 資源タイプ | conference object | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 著者 |
Sato, Katsutoshi
× Sato, Katsutoshi× Shintani, Yasushi× Takahashi, Sayaka× Nakanowatari, Keisuke× Teshima, Teruki× Matsuura, Nariaki× 佐藤 克俊× 手島 昭樹× 松浦 成昭 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Cancer cell that relapsed after radiotherapy must acquires radioresistance, but the mechanisms of acquired radioresistance in cancer cell are not fully understood. To investigate the mechanisms of acquired radioresistance in cancer cell, we irradiated the human adenocarcinoma cell line A549 with 2Gy of X-ray, repeated the irradiation 30 times, and established the radioresistant cancer cell line A549R. To evaluate the differences in the radioseisitivity, apoptosis and senescence induction between A549 and A549R, we performed colony formation assay, JC-1 staining, and X-gal staining, respectively. The results of colony formation assay showed that the survival fraction of A549R was significantly higher than that of A549. In addition, apoptosis and senescence induction in A549R were suppressed compared with that in A549. We further studied the DNA double strand break (DSB) repair potential in A549R. To measure the DSB repair potential, we performed the immunofluorescence staining with anti-gamma-H2AX, phosphorylated ataxia telangiectasia mutated (p-ATM) antibody at 1 to 3 days after X-ray irradiation and counted the focus number of gamma-H2AX and p-ATM in the nucleus. As a result, the disappearance of colocalized focus of gamma-H2AX and p-ATM in A549R was earlier than that in A549. These data showed that the repeated X-ray irradiation generates the radioresistant cancer cells that acquire the promotion of DSB repair potential. Next, we evaluated the difference in cell cycle progression and cell proliferation after X-ray irradiation between both cell lines. As a result, the percentage of G0/G1 phase in A549R was significantly higher than that in A549. Moreover, the cell proliferation in A549R after X-ray irradiation was suppressed compared with that in A549. Subsequently, we assessed the protein expression of p53 and p53-related proteins such as Bax, Puma, p21, and cyclin D1 by western blotting. The results showed that the p53 and cyclin D1 expression in A549R was suppressed compared with that in A549, but Bax, Puma, and p21 was not changed.We further assessed whether epithelial to mesenchymal transition (EMT) in A549R because it is known that EMT is closely associated with chemoresistance in cancer cell. As we expected, the cadherin switching was clearly observed in A549R. In this report, we will discuss the relationship between the radioresistance after X-ray irradiation, changes in DNA repair potential, and EMT induction. | |||||
| 会議概要（会議名, 開催地, 会期, 主催者等） | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 8th International Symposium of Cancer Research and Therapy | |||||
| 発表年月日 | ||||||
| 日付 | 2012-11-10 | |||||
| 日付タイプ | Issued | |||||
