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DEK function in silencing of Polycomb-target genes

ABSTRACT: Chromatin-bound protein DEK is potentially related to a DNA topology change. In Arabidopsis, mutations in the DEK genes enhance the aberrant morphology in the background of lhp1 (Like Heterochromatin Protein) mutant. LHP1 is responsible for the silencing of Polycomb target genes. We investigated whether defects in DEK genes affect transcriptional profiles in the presence and absence of the lhp1 mutation. Topoisomerase 1α is also known that affects DNA topology and interact with the DEK3 protein (Waidmann et al., 2014). ATRX is known as one of the LHP1 interacting proteins (Wang et al., 2018). By comparing these mutant transcriptomes, we addressed how these mutants are related to each other. We found that there is a synergistic effect on the misregulation of Polycomb target genes in the multiple mutant lhp1;dek2;3;4.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE175373 | GEO | 2025/10/15

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 function in silencing of Polycomb-target genes

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