BACH2 co binds with BCL6 to sets of genes involved in GC B-cell development including PRDM1. (A-B) Venn diagram representations illustrate the number of overlapping and unique target genes (A) and binding sites (B) of BACH2 and BCL6 identified by ChIP-seq in OCI-Ly7 cells. (C) QChIP was performed to determine enrichment of BCL6, BACH2, and MAFK at the indicated gene loci in OCI-LY7 (top panel) and primary human GC B cells (bottom panel). (D) Reciprocal coimmunoprecipitations were performed to detect the interaction of endogenous BCL6 and BACH2 in OCI-LY7 and primary human GC B cells. (E) The illustration depicts ChIP-seq tracks of BACH2, MAFK, and BCL6 at the PRDM1 locus. The transcription start sites of PRDM1α and PRDM1β are indicated by the arrows. Consensus DNA binding elements located at the major binding sites (B1 and B2) are shown at the bottom. (F) QChIP was performed to detect enrichment of BACH2 at B1 and B2 sites in Toledo DLBCL cell infected with a control virus (Ctrl) or virus expressing BCL6 (left panel), and reciprocally to detect BCL6 binding in Karpas422 DLBCL cells infected with a control (Ctrl) or virus expressing BACH2 (right panel). (G) qRT-PCR analysis was performed to assess the mRNA abundance of PRDM1α and PRDM1β in OCI-LY1 cells transfected with either scrambled non-specific short interfering RNA (siNT), BACH2 small interfering RNA (siRNA) (siBACH2#1), BCL6 siRNA (siBCL6#1), or siBACH2, together with siBCL6 after 72 hours. Data are presented as fold change of relative PRDM1 mRNA levels normalized to HPRT. Data are representative of 3 independent experiments (C,F,G). *P < .05; ns, not significant; 2-tailed Student t test.