دورية أكاديمية
The PI3K-Akt Pathway in SN-38-Induced Apoptosis in Human Gastric Cancer Cell Lines
العنوان: | The PI3K-Akt Pathway in SN-38-Induced Apoptosis in Human Gastric Cancer Cell Lines |
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المؤلفون: | Yoshioka Shizue, Tatebe Shigeru, Tokuyasu Naruo, Taniguchi Kenjiro, Ogami Yoshimi, Yamamoto Osamu, Ashida Keigo, Gomyo Yoshihito, Kondo Akira, Tsujitani Shunichi, Ikeguchi Masahide |
المصدر: | Yonago Acta medica. 2005, 48(1), 7-16 |
بيانات النشر: | Tottori University Faculty of Medicine |
سنة النشر: | 2005 |
المجموعة: | Tottori University Research Result Repository / 鳥取大学研究成果リポジトリ |
مصطلحات موضوعية: | apoptosis, gastric cancer, PI3K-Akt pathway, SN-38 |
الوصف: | SN-38, an active metabolite of a topoisomerase I inhibitor, CPT-11, exhibits a cytotoxic effect by inducing apoptosis in cancer cells. Phosphatidylinositol-3-OH kinase (PI3K)-Akt signaling is known to protect a variety of cells from apoptosis. The relationship between resistance to SN-38-induced apoptosis and the PI3K-Akt pathway in human gastric cancer cells is unknown. Here, we did an investigation using two gastric cancer cell lines, MKN1 and MKN45. Cell viability was determined by sodium 3'-[1-(phenylaminocarbonyl)-3,4-tetrazolium]-bis(4-methoxy-6-nitro) benzene sulfonic acid hydrate (XTT) assay. Apoptosis was confirmed by fluorescence microscopy using Hoechst 33342 staining. Expression levels of phospho-Akt (pAkt) were determined by Western blotting. After being treated with SN-38, the populations of sub-G1 cells were induced by flow cytometry in 36.8% of MKN45 cells more frequently than in 13.5% of MKN1 cells. SN-38 inhibited the expression of pAkt dose-dependently in MKN45 cells, but not in MKN1 cells. In MKN1 cells, an additional pretreatment with the PI3K inhibitor, LY294002, led to the inhibition of pAkt expression and induced apoptosis. The results suggested that SN-38 induces apoptosis by decreasing PI3K-Akt survival signaling, the anti-apoptotic signals, in human gastric cancer cells. Akt inhibitor might be a useful anti-tumor agent in combination with CPT-11. |
نوع الوثيقة: | article in journal/newspaper |
اللغة: | English |
تدمد: | 13468049 |
العلاقة: | https://repository.lib.tottori-u.ac.jp/?action=repository_uri&item_id=5076Test; http://id.nii.ac.jp/1824/00005070Test/; Yonago Acta medica = Yonago Acta medica, 48(1), 7-16(2005-03); AA00892882; https://repository.lib.tottori-u.ac.jp/?action=repository_action_common_download&item_id=5076&item_no=1&attribute_id=22&file_no=1Test |
الإتاحة: | http://id.nii.ac.jp/1824/00005070Test/ https://repository.lib.tottori-u.ac.jp/?action=repository_uri&item_id=5076Test https://repository.lib.tottori-u.ac.jp/?action=repository_action_common_download&item_id=5076&item_no=1&attribute_id=22&file_no=1Test |
حقوق: | Yonago Acta medica 編集委員会 |
رقم الانضمام: | edsbas.F8827AE8 |
قاعدة البيانات: | BASE |
تدمد: | 13468049 |
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