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Phase separation mediates AKAP95 regulating oncogenic MLL-fusion driven transcription and its application in leukemia therapy

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE271858 | GEO | 2025/11/11

REPOSITORIES: GEO

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Phase separation mediates AKAP95 regulating oncogenic MLL-fusion driven transcription and its application in leukemia therapy (PRO-Seq)

Project description:Oncogenic transcription represents a crucial event in MLL rearranged (MLLr) leukemia, yet the precise role of transcription co-activators in MLL-fusion protein-associated transcription and their contribution to leukemogenesis remain incompletely understood. Here, we demonstrate that AKAP95 is notably up-regulated in both MLLr patients and in MLL-AF9-transformed mouse bone marrow. AKAP95 proves essential for initiating mouse MLL-AF9 leukemia, exhibiting widespread DNA binding across the genome, particularly at gene promoters. Interaction with the translocated MLL1 fragment primarily occurs through phase separation mechanisms. AKAP95's RNA-binding properties, coupled with its phase separation behavior, govern its binding to pre-mRNA and concurrent transcriptional regulation. Importantly, we engineered a peptide to disrupt its phase separation, effectively attenuating AKAP95-mediated transcriptional co-activation and inhibiting the growth of MLLr cell lines. These findings illustrate a vivid example of an RNA-binding protein orchestrating transcription and tumorigenesis via phase separation, underscoring the potential for targeting oncogenic condensation mechanisms therapeutically.

2025-11-11 | GSE271856 | GEO

Phase separation mediates AKAP95 regulating oncogenic MLL-fusion driven transcription and its application in leukemia therapy (CLIP-Seq)

2025-11-11 | GSE271855 | GEO

Phase separation mediates AKAP95 regulating oncogenic MLL-fusion driven transcription and its application in leukemia therapy (ChIP-Seq)

2025-11-11 | GSE271854 | GEO

Phase separation mediates AKAP95 regulating oncogenic MLL-fusion driven transcription and its application in leukemia therapy (RNA-Seq)

2025-11-11 | GSE271857 | GEO

Phase separation mediates AKAP95 regulating oncogenic MLL-fusion driven transcription and its application in leukemia therapy

Project description:Phase separation mediates AKAP95 regulating oncogenic MLL-fusion driven transcription and its application in leukemia therapy

| PRJNA1133755 | ENA

Phase separation mediates AKAP95 regulating oncogenic MLL-fusion driven transcription and its application in leukemia therapy (ChIP-Seq)

Project description:Phase separation mediates AKAP95 regulating oncogenic MLL-fusion driven transcription and its application in leukemia therapy (ChIP-Seq)

| PRJNA1133759 | ENA

Phase separation mediates AKAP95 regulating oncogenic MLL-fusion driven transcription and its application in leukemia therapy (RNA-Seq)

Project description:Phase separation mediates AKAP95 regulating oncogenic MLL-fusion driven transcription and its application in leukemia therapy (RNA-Seq)

| PRJNA1133760 | ENA

Phase separation mediates AKAP95 regulating oncogenic MLL-fusion driven transcription and its application in leukemia therapy (CLIP-Seq)

Project description:Phase separation mediates AKAP95 regulating oncogenic MLL-fusion driven transcription and its application in leukemia therapy (CLIP-Seq)

| PRJNA1133758 | ENA

Phase separation mediates AKAP95 regulating oncogenic MLL-fusion driven transcription and its application in leukemia therapy (PRO-Seq)

Project description:Phase separation mediates AKAP95 regulating oncogenic MLL-fusion driven transcription and its application in leukemia therapy (PRO-Seq)

| PRJNA1133761 | ENA

Phase Separation Mediates NUP98 Fusion Oncoprotein Leukemic Transformation.

Project description:NUP98 fusion oncoproteins (FO) are drivers in pediatric leukemias and many transform hematopoietic cells. Most NUP98 FOs harbor an intrinsically disordered region from NUP98 that is prone to liquid-liquid phase separation (LLPS) in vitro. A predominant class of NUP98 FOs, including NUP98-HOXA9 (NHA9), retains a DNA-binding homeodomain, whereas others harbor other types of DNA- or chromatin-binding domains. NUP98 FOs have long been known to form puncta, but long-standing questions are how nuclear puncta form and how they drive leukemogenesis. Here we studied NHA9 condensates and show that homotypic interactions and different types of heterotypic interactions are required to form nuclear puncta, which are associated with aberrant transcriptional activity and transformation of hematopoietic stem and progenitor cells. We also show that three additional leukemia-associated NUP98 FOs (NUP98-PRRX1, NUP98-KDM5A, and NUP98-LNP1) form nuclear puncta and transform hematopoietic cells. These findings indicate that LLPS is critical for leukemogenesis by NUP98 FOs.SignificanceWe show that homotypic and heterotypic mechanisms of LLPS control NUP98-HOXA9 puncta formation, modulating transcriptional activity and transforming hematopoietic cells. Importantly, these mechanisms are generalizable to other NUP98 FOs that share similar domain structures. These findings address long-standing questions on how nuclear puncta form and their link to leukemogenesis. This article is highlighted in the In This Issue feature, p. 873.

| S-EPMC8983581 | biostudies-literature

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