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Priebe, V.

Publications and source records attributed to Priebe, V..

2 recordsLinked to original sources

The RNA helicase DDX21 cooperates with ETS1 and FLI1 in cell cycle, immune evasion, and snoRNA processing in activated B-cell-like diffuse large B-cell lymphoma cells

Diffuse large B-cell lymphoma (DLBCL) is a clinically and biologically heterogeneous disease, with the activated B-cell-like (ABC) subtype showing inferior outcomes. The ETS transcription factors ETS1 and FLI1 are recurrently gained and functionally relevant in DLBCL, yet their pathogenetic function is still to be fully elucidated. Here, we describe their cooperation with the RNA regulatory machinery, demonstrating that the RNA helicase DDX21 is a central effector of the ETS1/FLI1 transcriptional network in ABC-DLBCL. Our proteomic analyses revealed that ETS1 physically interacted with DDX21 and other RNA processing factors. As ETS1, DDX21 was preferentially expressed in ABC-DLBCL, particularly in the MCD/C5 genetic subtype, and it was associated with adverse clinical outcomes in this lymphoma subtype. Genetic and pharmacological studies demonstrated that DDX21 was essential for ABC-DLBCL cell proliferation. DDX21 also coordinated various transcriptional programs, which were revealed by integrated RNA-Seq, small RNA-Seq, ChIP-Seq, and Capture Hi-C analyses. DDX21-dependent transcription was relevant for ribosome biogenesis, MYC signaling, cell cycle progression, and immune evasion, but also regulated non-coding RNA networks, including microRNAs and small nucleolar RNAs, in particular SNORA37. Collectively, our data establish DDX21 as a nucleolar hub linking ETS transcription factors to coding and non-coding RNA programs that sustain aggressive lymphoma biology. These findings suggest DDX21 and ETS-RNA helicase complexes as promising therapeutic vulnerabilities in ABC-DLBCL.

cancer biology↗

TCF3::HLF Orchestrates an Enhancer-Promoter Network with Activation of MEF2C to Promote Immature HSC gene Expression in Leukemia

Oncogenic fusion transcription factors (TFs) frequently drive hematopoietic malignancies by altering gene expression in key developmental programs. TCF3::HLF is a fusion TF that characterizes a rare, treatment-resistant subtype of B-cell acute lymphoblastic leukemia (t(17;19) TCF3::HLF-positive B-ALL). Despite its clinical significance, the mechanisms by which TCF3::HLF induces leukemia are unclear. We used HiChIP mapping and genetic interference to analyze TCF3::HLF at the 3D-genome level, revealing enhancer-promoter interactions that control gene activation or repression. Notably, TCF3::HLF directly regulates MEF2C expression through its enhancer, as interference disrupted MEF2C transcription and inhibited leukemia propagation. This disruption also diminished embryonal hematopoietic stem cell (HSC) gene signatures and restored mature HSC and B-lymphoid markers. These findings highlight MEF2C as a critical component of the transcriptional network reprogrammed by TCF3::HLF. Our study provides insight into how TCF3::HLF rewires the 3D genome to drive leukemia and serves as a resource for further exploration of the TCF3::HLF regulome. TeaserUnraveling the 3D genomic interactions mediated by TCF3::HLF fusion protein in t(17;19) positive acute lymphoblastic leukemia.

cancer biology↗