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. 2017 May 12;7:1853. doi: 10.1038/s41598-017-01913-y

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Expression of ALOX5 is significantly down-regulated in MLL-rearranged AML. (a) Comparison of ALOX5 expression between t(11q23)/MLL-rearranged AML and AML cases with inv(16), t(8;21) or t(15;17), or normal controls (NC) in our in-house AML dataset^27–29. (b) Comparison of ALOX5 expression between t(11q23) AML and other subtypes of AML cases in GSE14468³⁰. The expression values were log2-transformed and mean centered. The P values were detected by t-test. (c,d) Downregulation of Alox5 in MLL-AF9-AML mouse BM mononuclear cells, as compared with normal controls. Levels of Alox5 were detected through qPCR (c) and Western blotting (d). (e–g) EZH2 and SIN3A bind the promoter of ALOX5. Enrichment of MLL-N terminal (for both wild-type MLL and MLL fusions), MLL-C terminal (for wild-type MLL), EZH2, SIN3A, H3K27me3 or IgG at the ALOX5 promoter region was shown. Relative to transcription start site of ALOX5, locations of the three PCR amplicon sites are: ALOX5-A (e): −522~−234 bp; ALOX5-B (f): −259~−79 bp; ALOX5-C (g): +149~+596 bp³². *P < 0.05; **P < 0.01, two-tailed t-test.