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NFATc1 regulates the transcription of DNA damage-induced apoptosis suppressor

DNA damage induced apoptosis suppressor (DDIAS), or human Noxin (hNoxin), is strongly expressed in lung cancers. DDIAS knockdown induced apoptosis in non-small cell lung carcinoma A549 cells in response to DNA damage, indicating DDIAS as a potential therapeutic target in lung cancer. To understand t...

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Detalles Bibliográficos
Autores principales: Im, Joo-Young, Lee, Kang-Woo, Won, Kyoung-Jae, Kim, Bo-Kyung, Ban, Hyun Seung, Yoon, Sung-Hoon, Lee, Young-Ju, Kim, Young-Joo, Song, Kyung-Bin, Won, Misun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4675896/
https://www.ncbi.nlm.nih.gov/pubmed/26740967
http://dx.doi.org/10.1016/j.dib.2015.11.011
Descripción
Sumario:DNA damage induced apoptosis suppressor (DDIAS), or human Noxin (hNoxin), is strongly expressed in lung cancers. DDIAS knockdown induced apoptosis in non-small cell lung carcinoma A549 cells in response to DNA damage, indicating DDIAS as a potential therapeutic target in lung cancer. To understand the transcriptional regulation of DDIAS, we determined the transcription start site, promoter region, and transcription factor. We found that DDIAS transcription begins at nucleotide 212 upstream of the DDIAS translation start site. We cloned the DDIAS promoter region and identified NFAT2 as a major transcription factor (Im et al., 2016 [1]). We demonstrated that NFATc1 regulates DDIAS expression in both pancreatic cancer Panc-1 cells and lung cancer cells.