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KDM6B protects T-ALL cells from NOTCH1-induced oncogenic stress

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

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE214576 | GEO | 2022/10/01

REPOSITORIES: GEO

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KDM6B protects T-ALL cells from NOTCH1-induced oncogenic stress.

Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematopoietic neoplasm resulting from the malignant transformation of T-cell progenitors. While activating NOTCH1 mutations are the dominant genetic drivers of T-ALL, epigenetic dysfunction plays a central role in the pathology of T-ALL and can provide alternative mechanisms to oncogenesis in lieu of or in combination with genetic mutations. The histone demethylase enzyme KDM6A (UTX) is also recurrently mutated in T-ALL patients and functions as a tumor suppressor. However, its gene paralog, KDM6B (JMJD3), is never mutated and can be significantly overexpressed, suggesting it may be necessary for sustaining the disease. Here, we used mouse and human T-ALL models to show that KDM6B is required for T-ALL development and maintenance. Using NOTCH1 gain-of-function retroviral models, mouse cells genetically deficient for Kdm6b were unable to propagate T-ALL. Inactivating KDM6B in human T-ALL patient cells by CRISPR/Cas9 showed KDM6B-targeted cells were significantly outcompeted over time. The dependence of T-ALL cells on KDM6B was proportional to the oncogenic strength of NOTCH1 mutation, with KDM6B required to prevent stress-induced apoptosis from strong NOTCH1 signaling. These studies identify a crucial role for KDM6B in sustaining NOTCH1-driven T-ALL and implicate KDM6B as a novel therapeutic target in these patients.

| S-EPMC10081958 | biostudies-literature

KDM6B protects T-ALL cells from NOTCH1-induced oncogenic stress [Mouse RNAseq]

Project description:Kdm6b mutant cells are at a survival disadvantage in NOTCH1- induced T-ALL

2022-10-01 | GSE214575 | GEO

KDM6B protects T-ALL cells from NOTCH1-induced oncogenic stress [Human RNAseq]

Project description:Kdm6b mutant cells are at a survival disadvantage in NOTCH1- induced T-ALL

2022-10-01 | GSE214573 | GEO

KDM6B protects T-ALL cells from NOTCH1-induced oncogenic stress

Project description:KDM6B protects T-ALL cells from NOTCH1-induced oncogenic stress

| PRJNA885884 | ENA

Shear Stress and NOTCH1 Regulate Calcification Related Genes in Human Aortic Valve Endothelium

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

2015-05-16 | E-GEOD-47160 | biostudies-arrayexpress

Tcf1 is essential for initiation of oncogenic Notch1-driven chromatin topology.

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

2022-01-21 | GSE169121 | GEO

KDM6B protects T-ALL cells from NOTCH1-induced oncogenic stress [Mouse RNAseq]

Project description:KDM6B protects T-ALL cells from NOTCH1-induced oncogenic stress [Mouse RNAseq]

| PRJNA885888 | ENA

KDM6B protects T-ALL cells from NOTCH1-induced oncogenic stress [Human RNAseq]

Project description:KDM6B protects T-ALL cells from NOTCH1-induced oncogenic stress [Human RNAseq]

| PRJNA885887 | ENA

Cdc73 protects Notch-induced T-cell leukemia cells from DNA damage and mitochondrial stress

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

2023-08-29 | GSE221345 | GEO

Cyclodextrin protects podocytes in diabetic kidney disease.

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

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