Cancer Genetics and Epigenetics 2024, Vol.12, No.6, 329-345 http://medscipublisher.com/index.php/cge 337 disassembly, thereby controlling the accessibility of chromatin to transcriptional machinery (Farooqi et al., 2020). In ovarian cancer, mutations or alterations in the components of these complexes can lead to defective chromatin remodeling, resulting in the dysregulation of ncRNA expression. The interaction between ncRNAs and chromatin remodeling complexes is a key mechanism by which ncRNAs exert their regulatory functions. For instance, lncRNAs can act as scaffolds to recruit chromatin-modifying enzymes to specific genomic loci, thereby influencing the epigenetic landscape and gene expression (Anastasiadou et al., 2017; Morlando and Fatica, 2018). This interaction is crucial for the regulation of genes involved in cell proliferation, apoptosis, and metastasis, highlighting the importance of chromatin remodeling in ncRNA-mediated cancer progression. 6.3 Examples of chromatin remodelers: specific complexes affecting ncRNA transcription Several chromatin remodelers have been identified to specifically affect ncRNA transcription in ovarian cancer. The SWI/SNF complex, for example, is known to play a significant role in the regulation of ncRNA expression. Mutations in the components of the SWI/SNF complex, such as ARID1A, have been frequently observed in ovarian cancer and are associated with altered chromatin states and dysregulated ncRNA transcription (Farooqi et al., 2020). These mutations can lead to the loss of chromatin accessibility at tumor suppressor gene loci, resulting in their silencing and promoting tumorigenesis. Another important chromatin remodeler is the polycomb repressive complex (PRC), which includes PRC1 and PRC2. These complexes are involved in the maintenance of repressive chromatin states through histone modifications such as H3K27me3. In ovarian cancer, overexpression of PRC2 components, such as EZH2, has been linked to the repression of tumor suppressor lncRNAs, thereby facilitating cancer cell proliferation and survival (Figure 3) (Forrest and Khalil, 2017; Farooqi et al., 2020). The interaction between PRC complexes and ncRNAs is critical for the regulation of gene expression programs that drive cancer progression. Figure 3 PRDM14 recruits Polycomb repressive complexes (PRC2) to represses expression of de novo DNA methyltransferases Histone deacetylases (HDACs) are another group of chromatin remodelers that play a crucial role in ncRNA regulation. HDACs remove acetyl groups from histones, leading to chromatin condensation and transcriptional repression. In ovarian cancer, the overexpression of HDACs has been associated with the silencing of tumor suppressor miRNAs and lncRNAs, contributing to the malignant phenotype (Kaikkonen et al., 2011; Farooqi et al., 2020). Inhibitors of HDACs are currently being explored as potential therapeutic agents to reactivate the expression of these ncRNAs and suppress tumor growth. Chromatin remodeling complexes such as SWI/SNF, PRC, and HDACs are key regulators of ncRNA transcription in ovarian cancer. Their dysregulation can lead to significant alterations in the epigenetic landscape, promoting cancer progression through the aberrant expression of ncRNAs. Understanding the interplay between chromatin remodelers and ncRNAs is essential for developing targeted therapies aimed at restoring normal gene expression patterns in ovarian cancer. 7 Non-coding RNA-Mediated Gene Silencing in Ovarian Cancer
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