Interleukin Enhancer-binding Factor 3/NF110 Is a Target of YM155, a Suppressant of Survivin

Survivin is responsible for cancer progression and drug resistance in many types of cancer. YM155 selectively suppresses the expression of survivin and induces apoptosis in cancer cells in vitro and in vivo. However, the mechanism underlying these effects of YM155 is unknown. Here, we show that a tr...

Descripción completa

Detalles Bibliográficos
Autores principales: Nakamura, Naoto, Yamauchi, Tomohiro, Hiramoto, Masashi, Yuri, Masatoshi, Naito, Masanori, Takeuchi, Masahiro, Yamanaka, Kentaro, Kita, Aya, Nakahara, Takahito, Kinoyama, Isao, Matsuhisa, Akira, Kaneko, Naoki, Koutoku, Hiroshi, Sasamata, Masao, Yokota, Hiroyuki, Kawabata, Shigeki, Furuichi, Kiyoshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The American Society for Biochemistry and Molecular Biology 2012
Materias:
Research
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3394938/
https://www.ncbi.nlm.nih.gov/pubmed/22442257
http://dx.doi.org/10.1074/mcp.M111.013243
Descripción
Sumario:Survivin is responsible for cancer progression and drug resistance in many types of cancer. YM155 selectively suppresses the expression of survivin and induces apoptosis in cancer cells in vitro and in vivo. However, the mechanism underlying these effects of YM155 is unknown. Here, we show that a transcription factor, interleukin enhancer-binding factor 3 (ILF3)/NF110, is a direct binding target of YM155. The enhanced survivin promoter activity by overexpression of ILF3/NF110 was attenuated by YM155 in a concentration-dependent manner, suggesting that ILF3/NF110 is the physiological target through which YM155 mediates survivin suppression. The results also show that the unique C-terminal region of ILF3/NF110 is important for promoting survivin expression and for high affinity binding to YM155.

Ejemplares similares