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. 2012 Oct 10;7(10):e46985. doi: 10.1371/journal.pone.0046985

Figure 4. Model for DEK transcriptional up-regulation following 17β-estradiol exposure.

Figure 4

Upon 17β-estradiol exposure, ERα is activated and binds to the DEK promoter at least at two locations – an ERE half site at −716 bp and at ERα/Sp1 binding sites more proximal to the transcriptional start site. A second potential mechanism of up-regulation is the ERα-mediated up-regulation of E2F proteins (particularly E2F3) that also increase DEK transcription. Increased levels of DEK then promote proliferation. DEK expression can be targeted with the anti-estrogen tamoxifen to inhibit cell proliferation. The knockdown of DEK by RNAi can increase tamoxifen sensitivity of ER+ cell lines by synergistically inducing an apoptotic response.