WEKO3
アイテム
Hepatitis B virus X protein overcomes oncogenic RAS-induced senescence in human immortalized cells
http://hdl.handle.net/2297/45958
http://hdl.handle.net/2297/459583ef4f3cf-02b6-4080-83d5-e89d28326da9
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
ME-PR-KANEKO-S-1540.pdf (702.8 kB)
|
|
| Item type | 学術雑誌論文 / Journal Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2017-10-03 | |||||
| タイトル | ||||||
| タイトル | Hepatitis B virus X protein overcomes oncogenic RAS-induced senescence in human immortalized cells | |||||
| 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_6501 | |||||
| 資源タイプ | journal article | |||||
| 著者 |
Oishi, Naoki
× Oishi, Naoki× Shilagardi, Khurts× Nakamoto, Yasunari× Honda, Masao× Kaneko, Shuichi× Murakami, Seishi |
|||||
| 提供者所属 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 医薬保健研究域医学系 | |||||
| 書誌情報 |
Cancer Science 巻 98, 号 10, p. 1540-1548, 発行日 2007-01-01 |
|||||
| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 1347-9032 | |||||
| NCID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA11808050 | |||||
| DOI | ||||||
| 関連タイプ | isIdenticalTo | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1111/j.1349-7006.2007.00579.x | |||||
| 出版者 | ||||||
| 出版者 | Japanese Cancer Association / Blackwell Publishing Ltd | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Chronic infection with hepatitis B virus (HBV) is a major risk factor for hepatocellular carcinoma. The HBV X protein (HBx) is thought to have oncogenic potential, although the molecular mechanism remains obscure. Pathological roles of HBx in the carcinogenic process have been examined using rodent systems and no report is available on the oncogenic roles of HBx in human cells in vitro. We therefore examined the effect of HBx on immortalization and transformation in human primary cells. We found that HBx could overcome active RAS-induced senescence in human immortalized cells and that these cells could form colonies in soft agar and tumors in nude mice. HBx alone, however, could contribute to neither immortalization nor transformation of these cells. In a population doubling analysis, an N-terminal truncated mutant of HBx, HBx-D1 (amino acids 51-154), which harbors the coactivation domain, could overcome active RAS-induced cellular senescence, but these cells failed to exhibit colonigenic and tumorigenic abilities, probably due to the low expression level of the protein. By scanning a HBx expression library of the clustered-alanine substitution mutants, the N-terminal domain was found to be critical for overcoming active RAS-induced senescence by stabilizing full-length HBx. These results strongly suggest that HBx can contribute to carcinogenesis by overcoming active oncogene-induced senescence. © 2007 Japanese Cancer Association. | |||||
| 権利 | ||||||
| 権利情報 | © Japanese Cancer Association 日本癌学会 | |||||
| 著者版フラグ | ||||||
| 出版タイプ | VoR | |||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
| 関連URI | ||||||
| 識別子タイプ | URI | |||||
| 関連識別子 | http://www.jca.gr.jp/ | |||||
