ALKBH8 promotes bladder cancer growth and progression through regulating the expression of survivin
| Autor: | Kentaro Jingushi, Tomoki Shimanoe, Hiroaki Hase, Yohei Tsukada, Kazuhiro Nakajima, Ryoji Kawakami, Yasuka Saigo, Kaori Kitae, Ikumi Ohshio, Yuko Ueda, Kazutake Tsujikawa |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Genetically modified mouse Survivin Biophysics Apoptosis Mice Transgenic Biology urologic and male genital diseases Biochemistry Inhibitor of Apoptosis Proteins Mice 03 medical and health sciences 0302 clinical medicine Cell Line Tumor medicine Animals Humans Molecular Biology Gene knockdown Bladder cancer Cell Biology medicine.disease XIAP 030104 developmental biology Urinary Bladder Neoplasms Tumor progression 030220 oncology & carcinogenesis NOX1 Immunology Disease Progression Cancer research AlkB Homolog 8 tRNA Methyltransferase |
| Zdroj: | Biochemical and Biophysical Research Communications. 477:413-418 |
| ISSN: | 0006-291X |
| DOI: | 10.1016/j.bbrc.2016.06.084 |
| Popis: | Human AlkB homolog 8 (ALKBH8) is highly expressed in high-grade, superficially and deeply invasive bladder cancer. Moreover, ALKBH8 knockdown induces apoptosis in bladder cancer cells. However, the underlying anti-apoptotic mechanism of ALKBH8 in bladder cancer cells has thus far remained unclear. Moreover, there is no direct evidence that highly expressed ALKBH8 is involved in tumor progression in vivo. We here show that ALKBH8 knockdown induced apoptosis via downregulating the protein expression of survivin, an anti-apoptotic factor also exhibiting increased levels in bladder cancer. We also clarify that ALKBH8 transgenic mice showed an accelerated rate of bladder tumor mass and invasiveness in an N-butyl-N-(4-hydroxybutyl)-nitrosamine-induced bladder cancer model. These findings suggest that the high expression of ALKBH8 is critical for the growth and progression of bladder cancer. |
| Databáze: | OpenAIRE |
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