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. 2022 Jun 30;20:296. doi: 10.1186/s12967-022-03476-7

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© The Author(s) 2022

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. 5 — SPOP-CHAF1A axis controls tumor autophagy of DLBCL in a TFEB-dependent manner. A Positive associations between CHAF1A and TFEB expressions based on TCGA-DLBCL samples. B The RT-qPCR assay showed that CHAF1A OE could promote TFEB expression (left), while CHAF1A KD reduced TFEB mRNA levels (right panel). C The ChIP-qPCR of H3K27ac markers and CHAF1A in promoter of TFEB gene in U2932 cells, as indicated (N = 4). D The RT-qPCR assay showed that CHAF1A KD could suppress TFEB transcriptional activity in U2932 cells (left panel) and FARAGE cells (middle panel). Relative luciferase activities were normalized versus control. The OCI-Ly7 cells were transfected with TFEB reporters together with TFEB vectors alone or TFEB + CHAF1A plasmids to show the regulation of TFEB reporter activity by CHAF1A (right panel). E Western blotting assay showed that CHAF1A-KD decreased the levels of autophagy-related markers (p62, and Beclin-1) in CHAF1A-silenced U2932 and FARAGE cells relative to control cells. F-G The luciferase activity (F) and mRNA levels (G) of lysosomal genes were measured in control and SPOP-OE OCI-Ly7 cells transfected with siCtrl or siTFEB, individually. H The tumor growth curves were obtained from OCI-Ly7-derived tumor models to show that targeting TFEB significantly suppressed the enhanced tumor growth induced by SPOP deficiency. I The tumor weight of mice from indicated groups was shown and compared. Experiments were performed in triplicate. *p < 0.05, **p < 0.01, ***p < 0.001