Background:The collaboration between the Polycomb Repressive Complex 2 (PRC2, an epigenetic modifier) and long non-coding RNAs (lncRNAs) has become a paradigm for gene regulation studies. In cancer cells, the MALAT1 lncRNA has arisen as a key partner for PRC2. However, it is unknown whether this partnership occurs genome-wide at the chromatin level, as most of the studies focus on single -usually repressed- genes. Due to the genomic binding properties of both macromolecules, we wondered whether there are binding sites shared by PRC2 and MALAT1. Results: Using public genome-binding datasets for PRC2 and MALAT1 derived from independent ChIP- and CHART-seq experiments performed in the breast cancer cell line MCF7, we searched for regions containing PRC2 and MALAT1 overlapping peaks. Peak calls for each molecule were performed using MACS2 and then overlapping peaks were identified by bedtools intersect. Using this approach, we identified 1,293 genomic sites where PRC2 and MALAT1 concur. Interestingly, 54,75% of those sites are within gene promoter regions (<3000 bases from the TSS). These analyses were also linked with transcription profiles of MCF7 cells, obtained from public RNA-seq data. Hence, it was determined that MALAT1 and PRC2 can concomitantly bind to promoters of genes that are actively transcribed in MCF7 cells. Gene ontology analyses revealed an enrichment of genes related to categories including cancer malignancy and epigenetic regulation. Conclusions: By re-visiting occupancy and transcriptomic data we identified a novel subset of genes, including key cancer-related genes, where MALAT1 and PRC2 may collaborate to control transcription.
In cancer cells, the long non-coding RNA (lncRNA) MALAT1 has arisen as a key partner for the Polycomb Repressive Complex 2 (PRC2), an epigenetic modifier. However, it is unknown whether this partnership occurs genome-wide at the chromatin level, as most of the studies focus on single genes that are usually repressed. Due to the genomic binding properties of both macromolecules, we wondered whether there are binding sites shared by PRC2 and MALAT1. Using public genome-binding datasets for PRC2 and MALAT1 derived from independent ChIP- and CHART-seq experiments performed with the breast cancer cell line MCF7, we searched for regions containing PRC2 and MALAT1 overlapping peaks. Peak calls for each molecule were performed using MACS2 and then overlapping peaks were identified by bedtools intersect. Using this approach, we identified 1293 genomic sites where PRC2 and MALAT1 concur. Interestingly, 54.75% of those sites are within gene promoter regions (<3000 bases from the TSS). These analyses were also linked with the transcription profiles of MCF7 cells, obtained from public RNA-seq data. Hence, it is suggested that MALAT1 and PRC2 can concomitantly bind to promoters of actively-transcribed genes in MCF7 cells. Gene ontology analyses revealed an enrichment of genes related to categories including cancer malignancy and epigenetic regulation. Thus, by re-visiting occupancy and transcriptomic data, we identified a key gene subset controlled by the collaboration of MALAT1 and PRC2.
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