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A dual role for PSIP1/LEDGF in T-cell acute lymphoblastic leukemia

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

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE253143 | GEO | 2024/10/20

REPOSITORIES: GEO

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Similar Datasets

A dual role for PSIP1/LEDGF in T cell acute lymphoblastic leukemia.

Project description:T cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy. Current intensified therapeutic protocols coincide with severe side effects, and no salvage therapy is available for primary therapy-resistant or relapsed patients. This highlights the need to identify new therapeutic targets in T-ALL. PSIP1, dispensable for normal hematopoiesis, is a dependency factor in KMT2A-rearranged myeloid leukemia. Nonetheless, loss-of-function mutations suggest a tumor suppressor role for PSIP1 in T-ALL. Here, we demonstrate that the loss of Psip1 accelerates T-ALL initiation in mice which we correlated with reduced H3K27me3 binding. Contrastingly, loss of PSIP1 impaired cell proliferation in several T-ALL cell lines. In cell lines, PSIP1 down-regulation leads to a reduction of COX20, an assembly factor of the cytochrome c oxidase in the mitochondria, and to a reduction in mitochondrial respiration. This indicates that PSIP1 can exert a dual role in the context of T-ALL, either as a tumor suppressor gene during tumor initiation or as a dependency factor in tumor maintenance.

| S-EPMC11529709 | biostudies-literature

A dual role for PSIP1/LEDGF in T-cell acute lymphoblastic leukemia [RNA-seq]

Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy. Although intensified therapeutic protocols have improved the outcome of T-ALL patients, they coincide with severe short- and long-term side effects. In addition, no salvage therapeutic strategies are available for primary therapy-resistant or relapsed T-ALL, resulting in a dismal outcome for these patients. It highlights the need to identify new targets in T-ALL biology that allow the development of less toxic targeted therapies. PSIP1, a histone mark reader, is a dependency factor in KMT2A-rearranged myeloid leukemia, but is dispensable for normal hematopoiesis, making it an attractive therapeutic target. Nonetheless, rare recurrent inactivating mutations and deletions of PSIP1, suggest that PSIP1 could act as a tumor suppressor in T-ALL. Here, we demonstrate that the loss of Psip1 accelerates T-ALL initiation in mice and we identified a correlation with reduced H3K27me3 binding. Contrastingly, loss of PSIP1 impaired cell proliferation in several human and murine T-ALL cell lines. In these cell lines, PSIP1 loss leads to a significant downregulation of COX20, an assembly factor of the cytochrome c oxidase in the mitochondria, and is associated with a reduction in mitochondrial respiration. Similarly to what was observed for PSIP1, loss of COX20 expression also leads to an impairment of proliferation in these T-ALL cell lines. These data corroborate that PSIP1 can exert a dual role in the context of T-ALL, either as a tumor suppressor gene during tumor initiation or as a dependency factor in tumor maintenance.

2024-10-20 | GSE253138 | GEO

A dual role for PSIP1/LEDGF in T-cell acute lymphoblastic leukemia [CUT&RUN]

2024-10-20 | GSE253137 | GEO

A dual role for PSIP1/LEDGF in T-cell acute lymphoblastic leukemia

Project description:A dual role for PSIP1/LEDGF in T-cell acute lymphoblastic leukemia

| PRJNA1064104 | ENA

A dual role for PSIP1/LEDGF in T-cell acute lymphoblastic leukemia [CUT&RUN]

Project description:A dual role for PSIP1/LEDGF in T-cell acute lymphoblastic leukemia [CUT&RUN]

| PRJNA1064101 | ENA

A dual role for PSIP1/LEDGF in T-cell acute lymphoblastic leukemia [RNA-seq]

Project description:A dual role for PSIP1/LEDGF in T-cell acute lymphoblastic leukemia [RNA-seq]

| PRJNA1064102 | ENA

Acute lymphoblastic leukemia

Project description:This SuperSeries is composed of the SubSeries listed below.

2010-09-10 | GSE24001 | GEO

PSIP1/LEDGF reduces R-loops at transcription sites and maintain genome integrity

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-12-08 | GSE220234 | GEO

Tumor suppressor role of Ezh2 in an NRASQ61K driven model of Early T-cell Precursor Acute Lymphoblastic Leukemia

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-01-07 | E-GEOD-76603 | biostudies-arrayexpress

Genome-wide chromatin maps of T-cell acute lymphoblastic leukemia (T-ALL)

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-03-01 | E-GEOD-54380 | biostudies-arrayexpress

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