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. 2019 Jul 18;27(2):695–710. doi: 10.1038/s41418-019-0381-y

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© The Author(s) 2019

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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Fig. 10 — A working model for PVT1-regulated NPC tumorigenesis. PVT1 acts as a scaffold of KAT2A and WDR5, and KAT2A promotes H3K9 acetylation and association with TIF1β, leading to increased NF90 transcription and HIF-1α stabilization, thus resulting in enhanced NPC tumorigenesis