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An epigenomic approach to identifying differential overlapping and cis-acting lncRNAs in cisplatin-resistant cancer cells [BiSulfite-seq]

ABSTRACT: An epigenomic approach to identifying differential overlapping and cis-acting lncRNAs in cisplatin-resistant cancer cells [BiSulfite-seq]

PROVIDER: PRJNA430411 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6500880_1.fastq.gz	Fastqsanger.gz
	SRR6500880_2.fastq.gz	Fastqsanger.gz
	SRR6500881_1.fastq.gz	Fastqsanger.gz
	SRR6500881_2.fastq.gz	Fastqsanger.gz
	SRR6500882_1.fastq.gz	Fastqsanger.gz

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An epigenomic approach to identifying differential overlapping and cis-acting lncRNAs in cisplatin-resistant cancer cells [BiSulfite-seq]

Project description:Long noncoding RNAs are critical regulators of cell biology whose alteration can lead to the development of diseases such as cancer. The potential role of lncRNAs and their epigenetic regulation in response to platinum treatment is largely unknown. We analyzed four paired cisplatin-sensitive/resistant non-small cell lung cancer and ovarian cancer cell lines. The epigenetic landscape of overlapping and cis-acting lncRNAs was determined by combining human microarray data on 30,586 lncRNAs and 20,109 protein coding mRNAs with whole genome bisulfite sequencing. Selected candidate lncRNAs were further characterized by PCR, Gene-Ontology analysis and targeted bisulfite sequencing. Differential expression in response to therapy was observed more frequently in cis-acting compared to overlapping lncRNAs (78% vs 22%, fold change ≥1.5), while significantly altered methylation profiles were more commonly associated with overlapping lncRNAs (29% vs. 8%; p<0.001). Moreover, overlapping lncRNAs contain more CpG islands (CGIs) (25% vs. 17%) and the majority of CGI-containing overlapping lncRNAs share these CGIs with their associated coding genes (84%). The differences in expression between sensitive and resistant cell lines were replicated in 87% of the selected candidates (p<0.05), while our bioinformatics approach identifying differential methylation was confirmed in all of the selected lncRNAs (100%). Five lncRNAs under epigenetic regulation appear to be involved in cisplatin resistance (AC091814.2, AC141928.1, RP11-65J3.1-002, BX641110 and AF198444). These novel findings provide new insights into epigenetic mechanisms and acquired resistance to cisplatin that highlight specific lncRNAs, some with unknown function that may signal strategies in epigenetic therapies.

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An epigenomic approach to identifying differential overlapping and cis-acting lncRNAs in cisplatin-resistant cancer cells

Project description:An epigenomic approach to identifying differential overlapping and cis-acting lncRNAs in cisplatin-resistant cancer cells

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An epigenomic approach to identifying differential overlapping and cis-acting lncRNAs in cisplatin-resistant cancer cells

Project description:Long noncoding RNAs are newly discovered regulators that play a critical role in cell biology, crucial to the correct functioning of the cell. Alterations in lncRNAs can lead to the development of diseases such as cancer. However, the role of lncRNAs in resistance to platinum chemotherapy is largely unknown. To screen for epigenetic changes involved in the development of resistance, we combined lncRNA and mRNA expression microarrays with whole genome bisulfite sequencing (WGBS) in four paired cisplatin-sensitive/resistant cells from non-small cell lung cancer and ovarian cancer. We found low levels of expression changes in lncRNAs (1.5%) and mRNAs (2%) when comparing resistant vs. sensitive cells. The correlation between lncRNA/mRNA arrays and WGBS identified two groups of lncRNAs, classified according to their relationship with the gene they have in silico complementarity or with their possible epigenetic regulation at the DNA methylation level. Validation of the results of expression and methylation levels allowed us to characterize lncRNAs in cisplatin-resistant phenotypes. In this study, we characterized lncRNAs that change in cisplatin-resistant cells due to epigenetic regulation at the DNA methylation level and the associated changes in expression levels. We have identified two groups of differentially expressed and methylated lncRNAs, indicating a new approach to the study of the mechanisms involved in the development of acquired resistance to cisplatin in cancer cells.

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An epigenomic approach to identifying differential overlapping and cis-acting lncRNAs in cisplatin-resistant cancer cells.

Project description:Long noncoding RNAs (lncRNAs) are critical regulators of cell biology whose alteration can lead to the development of diseases such as cancer. The potential role of lncRNAs and their epigenetic regulation in response to platinum treatment are largely unknown. We analyzed four paired cisplatin-sensitive/resistant non-small cell lung cancer and ovarian cancer cell lines. The epigenetic landscape of overlapping and cis-acting lncRNAs was determined by combining human microarray data on 30,586 lncRNAs and 20,109 protein coding mRNAs with whole-genome bisulfite sequencing. Selected candidate lncRNAs were further characterized by PCR, gene-ontology analysis, and targeted bisulfite sequencing. Differential expression in response to therapy was observed more frequently in cis-acting than in overlapping lncRNAs (78% vs. 22%, fold change ?1.5), while significantly altered methylation profiles were more commonly associated with overlapping lncRNAs (29% vs. 8%; P value <0.001). Moreover, overlapping lncRNAs contain more CpG islands (CGIs) (25% vs. 17%) and the majority of CGI-containing overlapping lncRNAs share these CGIs with their associated coding genes (84%). The differences in expression between sensitive and resistant cell lines were replicated in 87% of the selected candidates (P<0.05), while our bioinformatics approach identifying differential methylation was confirmed in all of the selected lncRNAs (100%). Five lncRNAs under epigenetic regulation appear to be involved in cisplatin resistance (AC091814.2, AC141928.1, RP11-65J3.1-002, BX641110, and AF198444). These novel findings provide new insights into epigenetic mechanisms and acquired resistance to cisplatin that highlight specific lncRNAs, some with unknown function, that may signal strategies in epigenetic therapies.

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Highly conserved and cis-acting lncRNAs produced from paralogous regions in the center of HOXA and HOXB clusters in the endoderm lineage

Project description:Long noncoding RNAs (lncRNAs) have been shown to play important roles in gene regulatory networks acting in early development. There has been rapid turnover of lncRNA loci during vertebrate evolution, with few human lncRNAs conserved beyond mammals. The sequences of these rare deeply conserved lncRNAs are typically not similar to each other. Here, we characterize HOXA-AS3 and HOXB-AS3, lncRNAs produced from the central regions of the HOXA and HOXB clusters. Sequence-similar orthologs of both lncRNAs are found in multiple vertebrate species and there is evident sequence similarity between their promoters, suggesting that the production of these lncRNAs predates the duplication of the HOX clusters at the root of the vertebrate lineage. This conservation extends to similar expression patterns of the two lncRNAs, in particular in cells transiently arising during early development or in the adult colon. Functionally, the RNA products of HOXA-AS3 and HOXB-AS3 regulate the expression of their overlapping HOX5–7 genes both in HT-29 cells and during differentiation of human embryonic stem cells. Beyond production of paralogous protein-coding and microRNA genes, the regulatory program in the HOX clusters therefore also relies on paralogous lncRNAs acting in restricted spatial and temporal windows of embryonic development and cell differentiation.

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Differential Expression of LncRNAs after cisplatin treatment in tongue squamous carcinoma cells

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