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. 2022 Sep 3;13(9):763. doi: 10.1038/s41419-022-05208-7

Fig. 4. SMYD3 promotes PKM2 transcription and the malignant phenotype of DLBCL via H3K4me3.

Fig. 4

A DNA agarose gel electrophoresis following ChIP-PCR showing the binding region of SMYD3 2000 bp upstream/downstream of the TSS of PKM2.ChIP-qPCR assays showing the enrichment of SMYD3 (B) and H3K4me3 (C) at potential binding sites A, B, C and D of PKM2. D Protein expression levels of SMYD3 following overexpression of SMYD3 WT and ΔEEL in SMYD3-knockdown DLBCL cell lines. E, F PKM2 mRNA levels after overexpression of SMYD3 WT and ΔEEL in SMYD3-knockdown DLBCL cell lines. G, H The SMYD3 and H3K4me3 enrichment levels in the PKM2 regulatory regions after overexpression of SMYD3 WT and ΔEEL in SMYD3-knockdown OCI-LY8 cells. I SMYD3-knockdown OCI-LY1 and OCI-LY8 cells were transfected with SMYD3 WT or SMYD3 ΔEEL, and the proliferation rates were measured using Cell Counting Kit-8 assays. J Changes in glucose uptake, lactate production and pyruvate levels. *P < 0.05, **P < 0.01, ***P < 0.001. DLBCL Diffuse large B-cell lymphoma, SMYD3 SET and MYND domain containing 3, PKM2 Pyruvate kinase M2, TSS Transcription start site, ChIP Chromatin immunoprecipitation, qPCR Quantitative PCR, WT Wild-type.