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Long non-coding RNA UCA1 modulates chromatin remodeling via SMARCA2-containing SWI/SNF complex in human colorectal cancer

ABSTRACT: Differential lncRNA expression has been correlated to clinical characteristics of colorectal cancers (CRC), which are the second leading cause of cancer-related deaths. LncRNA UCA1 plays a role in epigenetic gene regulation in diverse cancers. We studied CRC cell properties in CRISPR/Cas9 HT29-derived models and, interestingly, UCA1-depleted HT29 cells presented an increased stem-cell phenotype. We show that loss of UCA1 modulates SWI/SNF chromatin remodeling complexes, which were previously shown to be involved in maintaining stem-cell properties. Not only was UCA1 permissive for induced SWI/SNF subunit SMARCA2 (BRM) expression upon chemo-drug treatment, but it also affected subunit compositions of SWI/SNF complexes by direct interaction of UCA1 with both ATP helicase BRM and BRG1. UCA1 is known to stimulate proliferation and decrease apoptosis, and we here show that it can restrain cells from a stem cell phenotype. The dual action of UCA1 revealed in this study highlights the complex actions of lncRNAs in cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE280932 | GEO | 2025/11/06

REPOSITORIES: GEO

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Project description:Switch defective/sucrose non-fermentable chromatin remodeling complexes are multi-subunit machines that play vital roles in regulating chromatin structure and gene expression. However, how SWI/SNF complexes recognize target loci is still not fully understood. Here, we show that Arabidopsis bromodomain-containing homologous proteins, BRD1, BRD2 and BRD13, are core subunits of SWI/SNF complexes that are required for SWI/SNF genomic targeting. The three BRDs directly interact with multiple SWI/SNF subunits, including the BRAHMA (BRM) catalytic subunit. Phenotypic and transcriptome analysis of the brd1 brd2 brd13 triple mutants showed that the BRDs act in large redundancy to control developmental processes and gene expression that are also regulated by BRM. BRDs extensively co-localize with BRM on chromatin. brd1 brd2 brd13 mutation results in the reduced BRM protein levels and genome-wide targeting on chromatin. Finally, we demonstrate that the bromodomain of BRD2 is essential for genomic targeting of BRD2, highlighting the role of this reader domain in the recruitment of BRM-containing SWI/SNF complexes to target sites in plants. SWI/SNF chromatin remodeling complexes are evolutionarily conserved and is confirmed to use the energy derived from hydrolysis of ATP to alter the density or the position of nucleosomes on the DNA or the composition of histone octamer. Bromodomain, an acetylated histone interaction module, was found in chromatin remodeling factors. During the 29 Arabidopsis bromodomain-containing protein, like GCN5 and GTE4/6, their function has been reported. Here, we reported three BRM-interacting bromodomain-containing protein, BRD1, BRD2 and BRD13 are new core subunits of Arabidopsis SWI/SNF complexes. brd1/2/13 displayed a similar phenotype like brm, such as down-ward curled leaves, reduced fertility, shorter silique and root. Moreover, brm brd1/2/13 shows more serious phenotype just like brm-1. Y2H, Co-IP, RNA-seq and ChIP-seq assay reveal that BRDs interact with BRM at both protein and chromatin level. Future more, BRDs are required for BRM genome-wide occupancy and BRM might bind to chromatin via BRDs bromodomain by interacting with their BBC domain.

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Long non-coding RNA UCA1 modulates chromatin remodeling via SMARCA2-containing SWI/SNF complex in human colorectal cancer

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