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. 2021 May 27;19:62. doi: 10.1186/s12964-021-00707-0

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Methylation of AATK/miR-1250 in healthy normal controls and NHL cell lines. a Schematic diagram showing the relative locations of miR-1250, AATK gene, CpG island, AATK qRT-PCR primer and amplicons of MSP. b Direct sequencing of AATK/miR-1250 M-MSP products from positive control with methylated DNA demonstrated complete bisulfite conversion and MSP specificity. c M- and U-MSP showed that AATK/miR-1250 was unmethylated in healthy normal controls, including normal peripheral blood buffy coats (P1–P10) and normal tonsil tissues (T1–T11). d In NHL cell lines, M- and U-MSP showed that AATK/miR-1250 was completely unmethylated (UU) in GRANTA-519, JEKO-1, MINO, REC-1 and SP-53, and completely methylated (MM) in SU-DHL-6, SU-DHL-16, KARPAS-299, SU-DHL-1 and SUP-T1