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Dissecting the interface between ARID1A and mRNA translation in bladder cancer

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

ORGANISM(S): Mus musculus

PROVIDER: GSE201222 | GEO | 2023/03/13

REPOSITORIES: GEO

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Dissecting the interface between ARID1A and mRNA translation in bladder cancer (Polysome)

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Dissecting the interface between ARID1A and mRNA translation in bladder cancer (CUT&Tag)

Project description:Chromatin remodeling and protein synthesis are tightly regulated processes that impact gene expression and cellular phenotypes. However, it is unknown if these two regulatory mechanisms are linked or exert independent effects in normal epithelial physiology and disease states. We have uncovered a new functional relationship between the chromatin remodeler ARID1A and mRNA translation elongation that is involved in maintaining cellular fitness in the context of bladder carcinogenesis. Loss of ARID1A triggers inhibition of the translation elongation factor eEF2 and ribosome accumulation, which results in a reduction in protein synthesis. In the setting of ARID1A deficiency the bladder carcinogen BBN induces DNA damage and cell death without impacting cancer initiation. As such, ARID1A is necessary for tumorigenesis. Remarkably, restoration of translation elongation through eEF2 is sufficient to initiate transformation in the context of ARID1A loss. However, dependence on ARID1A for transformation appears to be context specific, as loss of ARID1A after tumor establishment is sufficient for cancer progression.

2023-03-13 | GSE201220 | GEO

Dissecting the interface between ARID1A and mRNA translation in bladder cancer

Project description:Dissecting the interface between ARID1A and mRNA translation in bladder cancer

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Dissecting the interface between ARID1A and mRNA translation in bladder cancer (Polysome)

Project description:Dissecting the interface between ARID1A and mRNA translation in bladder cancer (Polysome)

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Dissecting the interface between ARID1A and mRNA translation in bladder cancer (CUT&Tag)

Project description:Dissecting the interface between ARID1A and mRNA translation in bladder cancer (CUT&Tag)

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DNA methylation and expression profiling study for bladder cancer

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

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

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

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Profiling of bladder cancer

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

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mRNA translation is a therapeutic vulnerability necessary for bladder epithelial transformation.

Project description:Using genetically engineered mouse models, this work demonstrates that protein synthesis is essential for efficient urothelial cancer formation and growth but dispensable for bladder homeostasis. Through a candidate gene analysis for translation regulators implicated in this dependency, we discovered that phosphorylation of the translation initiation factor eIF4E at serine 209 is increased in both murine and human bladder cancer, and this phosphorylation corresponds with an increase in de novo protein synthesis. Employing an eIF4E serine 209 to alanine knock-in mutant mouse model, we show that this single posttranslational modification is critical for bladder cancer initiation and progression, despite having no impact on normal bladder tissue maintenance. Using murine and human models of advanced bladder cancer, we demonstrate that only tumors with high levels of eIF4E phosphorylation are therapeutically vulnerable to eFT508, the first clinical-grade inhibitor of MNK1 and MNK2, the upstream kinases of eIF4E. Our results show that phospho-eIF4E plays an important role in bladder cancer pathogenesis, and targeting its upstream kinases could be an effective therapeutic option for bladder cancer patients with high levels of eIF4E phosphorylation.

| S-EPMC8262354 | biostudies-literature

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