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<Originals> Appropriate inhibition of autophagy after treatment with imatinib mesylate enhances cytotoxicity in malignant peripheral nerve sheath tumor cells
https://kindai.repo.nii.ac.jp/records/10559
https://kindai.repo.nii.ac.jp/records/10559aa84b3d5-121d-4924-9161-8e90d5bde372
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
AA0050842X-20130600-0045.pdf (3.3 MB)
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| Item type | ☆紀要論文 / Departmental Bulletin Paper(1) | |||||||||
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| 公開日 | 2013-09-16 | |||||||||
| タイトル | ||||||||||
| タイトル | <Originals> Appropriate inhibition of autophagy after treatment with imatinib mesylate enhances cytotoxicity in malignant peripheral nerve sheath tumor cells | |||||||||
| 言語 | en | |||||||||
| 著者 |
Okano, Munehiro
× Okano, Munehiro
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| 言語 | ||||||||||
| 言語 | eng | |||||||||
| キーワード | ||||||||||
| 主題 | malignant peripheral nerve sheath tumor, imatinib mesylate, platelet-derived growth factor receptor, autophagy | |||||||||
| 資源タイプ | ||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||||
| 資源タイプ | departmental bulletin paper | |||||||||
| 著者 所属 | ||||||||||
| 値 | Department of Pediatrics, Kinki University Faculty of Medicine | |||||||||
| 著者所属(翻訳) | ||||||||||
| 値 | 近畿大学医学部 | |||||||||
| 版 | ||||||||||
| 出版タイプ | VoR | |||||||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||||
| 出版者 名前 | ||||||||||
| 出版者 | The Kinki University Medical Association | |||||||||
| 書誌情報 |
en : ACTA MEDICA KINKI UNIVERSITY 巻 38, 号 1, p. 45-55, 発行日 2013-06-01 |
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| ISSN | ||||||||||
| 収録物識別子タイプ | ISSN | |||||||||
| 収録物識別子 | 03866092 | |||||||||
| 抄録 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | [Abstract] Malignant peripheral nerve sheath tumor (MPNST), which is very rare in childhood, is a highly aggressive soft tissue tumor that is refractory to conventional therapy. Since this tumor expresses platelet-derived growth factor receptor, imatinib mesylate may be a novel therapeutic option. However, cellular reactions after the treatment of MPNST with imatinib are not fully understood. Therefore, we investigated the cellular reactions of imatinib in vitro using three MPNST cell lines. Imatinib induced cytotoxicity in vitro with variable IC_<50> values (11.7-＞ 30μM). The induction of apoptosis was not a pivotal mechanism in the inhibitory effects. We found that the treatment of MPNST cell lines with imatinib induced autophagy. Suppression of the initiation of autophagy by 3-methyladenine or small interfering RNA (siRNA) against beclin-1 attenuated imatinib-mediated cytotoxicity. In contrast, blocking the formation of autophagosomes or development of autolysosomes using siRNA against microtubule-associated protein light chain 3B (LC3B) or bafilomycin Al enhanced imatinib-induced cytotoxicity in MPNST cells. Our data showed that imatinib-mediated autophagy can function as a cytotoxic mechanism and that appropriate modulation of autophagy may sensitize MPNST cells to imatinib, which in turn may be a novel therapeutic strategy for MPNST. | |||||||||
| フォーマット | ||||||||||
| 内容記述タイプ | Other | |||||||||
| 内容記述 | application/pdf | |||||||||
