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DEK controls the trade-off between growth and arrest via H2A.Z-nucleosomes in Arabidopsis

ABSTRACT: The decision of whether to grow and proliferate or to restrict growth and develop resilience to stress is a key biological trade-off. Multiple tumour suppressors have roles in suppressing growth and proliferation when conditions are unfavourable, and aggressive tumours show re-wiring of the metabolic pathways and removal of these restraints on growth1,2. In plants, constitutive growth results in increased sensitivity to environmental stress3,4. However, the underlying mechanisms controlling this decision are not well understood. We used temperature as a cue to discover regulators of this process in plants, as it both enhances growth and development rates within a specific range, and is also a stress at extremes. We find the conserved chromatin protein DEK plays a central role in balancing the response between growth and arrest in Arabidopsis, and it does this via H2A.Z-nucleosomes. DEK target genes show two distinct categories of chromatin architecture, and these predict induction or repression by DEK. We show that these chromatin signatures of DEK target genes might be conserved in human cells, suggesting that DEK may act through a fundamental evolutionarily conserved mechanism to control the balance between growth and arrest in plants and animals.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE114185 | GEO | 2024/05/01

REPOSITORIES: GEO

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Project description:Introduction: Neuroendocrine prostate cancer (NEPC) is an aggressive subtype of prostate cancer, exhibiting rapid progression and is unresponsive to hormone therapy. Reliable prognostic assays and more effective treatments are critically required. However, the research of NEPC has been hampered by a lack of clinically relevant in vivo models. Recently, we successfully developed a first-in-field patient tissue-derived xenograft model of complete neuroendocrine transdifferentiation from prostate adenocarcinoma. By comparing gene expression profiles of the parental adenocarcinoma line (LTL331) and the NEPC subline (LTL331R), we identified DEK, a gene not previously reported in prostate cancer, as a potential biomarker and target for NEPC. Methods: DEK protein expression in patient tissue-derived xenograft models and clinical samples was assessed by immunohistochemistry. The function of DEK was determined by siRNA-induced reduction of DEK expression in PC-3 cells, a cell line with NEPC characteristics, followed by functional assays and gene expression profiling analysis. Results: Elevated DEK protein expression was observed in all clinical NEPC cases, which is distinct from their benign counterparts (0%), hormonal naïve prostate cancer (2.45%) and castration resistant prostate cancer (29.55%). Increased DEK expression is an independent clinical risk factor and is associated with shorter disease free survival in hormonal naïve prostate cancer patients. Reduction of DEK expression in PC-3 cells led to a marked reduction in cell proliferation, cell migration and invasion. Conclusions: The results suggest that DEK may play an important role in the progression of prostate cancer, especially NEPC and provide a potential biomarker to aid risk stratification of prostate cancer and a novel therapeutic target for treating NEPC. The function of DEK was determined by siRNA-induced reduction of DEK expression in PC-3 cells, a cell line with NEPC characteristics, followed by functional assays and gene expression profiling analysis.

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DEK controls the trade-off between growth and arrest via H2A.Z-nucleosomes in Arabidopsis

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