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NFATc1 regulates the transcription of DNA damage-induced apoptosis suppressor

机译:NFATc1调节DNA损伤诱导的凋亡抑制因子的转录

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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 ). We demonstrated that NFATc1 regulates DDIAS expression in both pancreatic cancer Panc-1 cells and lung cancer cells.
机译:DNA损伤诱导的凋亡抑制因子(DDIAS)或人Noxin(hNoxin)在肺癌中强烈表达。 DDIAS敲低诱导非小细胞肺癌A549细胞的DNA损伤反应凋亡,表明DDIAS是肺癌的潜在治疗靶点。为了了解DDIAS的转录调控,我们确定了转录起始位点,启动子区域和转录因子。我们发现DDIAS转录开始于DDIAS翻译起始位点上游的核苷酸212。我们克隆了DDIAS启动子区域,并确定NFAT2是主要的转录因子(Im等,2016)。我们证明了NFATc1调节胰腺癌Panc-1细胞和肺癌细胞中的DDIAS表达。

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