Fig 2: NCAPD3 modulated the expression of SIRT1 in an H3K9me1-dependent manner. A) Co-IP assay showed NCAPD3 could not interact with the previously-reported histone methylation modifications, H3K4me3 and H4K20me1, in DLBCL. B) Co-IP assay verified that NCAPD3 and TFII I could interact with H3K9me1 in DLBCL. C) The location of TFII I and H3K9me1 at the SIRT1 promoter was proved by ChIP-PCR followed by southern blot. D) The level of H3K9me1 modifications at the SIRT1 promoter was downregulated in shNCAPD3 group as examined by ChIP-qRT-PCR assay. E) The mRNA of SIRT1 was highly expressed in DLBCL specimens (n = 55) than control specimens (n = 33) based on GSE56315. F) Patients in the SIRT1-high group suffered shorter OS based on GSE32918. G) The mRNA of SIRT1 was higher in DLBCL cell lines (OCI-LY1, OCI-LY3, OCI-LY8, OCI-LY10, Val and U2932) compared with normal CD19+ B cells. H) The transfection efficiency of SIRT1 overexpression plasmids was confirmed by immunoblotting. I) CCK-8 assay hinted that SIRT1 overexpression accelerated cell proliferation. J) No significant alteration in cell cycle was observed upon SIRT1 overexpression. K) Flow cytometric analysis indicated SIRT1 overexpression slightly inhibited apoptosis. (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001).