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. Author manuscript; available in PMC: 2016 Jun 28.
Published in final edited form as: Oncogene. 2014 Mar 31;34(10):1323–1332. doi: 10.1038/onc.2014.60

Figure 1.

Figure 1

STAT- and p53-binding sites are required for transcriptional activity of the LPP/miR-28 promoter. (a) The cloned DNA sequence corresponding to the LPP/miR-28 promoter (chr3:187 871 155–187 872 054) was tested for its promoting activity compared with an empty luciferase vector (*Po0.05) by transfection in human HEL cells, that express LPP/miR-28 from its endogenous locus. The mutant promoters Δ− 290 and Δ+188 expressed significantly less luciferase, demonstrating that the transcriptional activity of the original promoter require a STAT (Δ− 290) and a p53 (Δ+188) binding site. (b) Predicted consensus binding sites for known transcription factors were deleted individually by directed mutagenesis and tested for luciferase activity compared with the original promoter. (c) A p53 expressing vector was cotransfected in HEL cells with a luciferase reporter under the control of the LPP/miR-28 promoter. The transcriptional activity was significantly increased by the expression of p53 WT (*Po0.05). (d) The transcription in UT-7e cells via the LPP/miR-28 promoter was increased by p53 WT (*Po0.05) and in the presence of both STAT5 and p53 WT (*Po0.05), but not by the inactive p53 mutant (V143A). The average of two experiments performed in triplicates is represented. Error bars represent s.e.m.