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. Author manuscript; available in PMC: 2011 Jul 1.
Published in final edited form as: Gene. 2010 Mar 23;459(1-2):11–23. doi: 10.1016/j.gene.2010.03.006

Table 1.

Identification of the human AKR1C1 basal proximal promoter.

Fold increase in relative luciferase activity (RLA)
5’ Deletion Constructs HepG2 2008 2008/C13* H23 A549
pGL3 Easic 1 1 1 1 1
pAKRICI −88/+59 1.1 ± 0.2 1.4 ± 0.4 1.3 ± 0.8 1 ± 0.3 2.8 ± 1
pAKRICI −128/+59 4.5 ± 2.8 8.2 ± 0.6 3.3 ± 0.6 7.7 ± 1.0 22.0 ± 9.8
pAKRICI −152/+59 6.6 ± 2.0 - - - -
pAKRICI −180/+59 7.1 ± 2.5 10.5 ± 3.6 7.3 ± 1.0 10.7 ± 1.5 17.8 ± 1.7
pAKRICI −349/+59 8.8 ± 3.2 - - - -
pAKRICI −641/+59 11.2 ± 6.5 13.7 ± 2.6 11 ± 3.0 15.8 ± 3.0 33 ± 3.8
pAKRICI −1648/+59 11.0 ± 3.0 - - - -
pAKRICI −2301/+59 6.7 ± 1.6 - - - -
pAKRICI −2567Z+59 6.5 ± 1.7 - - - -
pAKRICI −2954/459 5.8 ± 1.8 13.5 ± 8.0 22.9 ± 8.5 36.4 ± 19.2 29.2 ± 1.8

Human liver carcinoma cells (HepG2), ovarian carcinoma cells (2008, 2008/C13*) were transfected with various AKR1C1 promoters constructs shown in Fig 1B and assayed for luciferase activity after 48h as described in Materials and Methods. Fold increase in relative luciferase activity (RLA) was compared with that observed with pGL3 basic (set as 1). Normalization in transfection efficiency was performed by co-transfection with pRL-SV40 (Renilla expression vector). The mean ± S.D are from three different experiments, each performed in triplicate.