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BORG-dependent alterations in the transcriptome of D2.OR cells

ABSTRACT: The ubiquitous nature of lncRNAs to comprehensively alter cellular transcriptional networks led us to hypothesize that BORG is capable of compelling metastasic, chemoresistant, and pro-survival activities in triple-negative breast cancers by inducing global transcriptomic reprogramming. As such, we performed RNA-seq to garner mechanistic insights into BORG-dependent pathways within D2.OR cells. Accordingly, transcriptional profiles associated with aggressive breast cancers and adaptive survival programs were amongst the top enriched pathways in BORG-expressing D2.OR cells. Most notably, BORG enriched for gene signatures that were critical for the development of chemoresistance towards doxorubicin, as well as a core set of genes upregulated in response to hypoxia, radiotherapy, and serum-deprivation.

ORGANISM(S): Mus musculus

PROVIDER: GSE116656 | GEO | 2019/03/27

REPOSITORIES: GEO

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Project description:Metaplastic breast cancers (MBC) are aggressive, chemoresistant tumors characterized by lineage plasticity. To advance understanding of their pathogenesis and relatedness to other breast cancer subtypes, 28 MBCs were compared with common breast cancers using comparative genomic hybridization, transcriptional profiling, and reverse-phase protein arrays and by sequencing for common breast cancer mutations. MBCs showed unique DNA copy number aberrations compared with common breast cancers. PIK3CA mutations were detected in 9 of 19 MBCs (47.4%) versus 80 of 232 hormone receptor-positive cancers (34.5%; P = 0.32), 17 of 75 HER-2-positive samples (22.7%; P = 0.04), 20 of 240 basal-like cancers (8.3%; P < 0.0001), and 0 of 14 claudin-low tumors (P = 0.004). Of 7 phosphatidylinositol 3-kinase/AKT pathway phosphorylation sites, 6 were more highly phosphorylated in MBCs than in other breast tumor subtypes. The majority of MBCs displayed mRNA profiles different from those of the most common, including basal-like cancers. By transcriptional profiling, MBCs and the recently identified claudin-low breast cancer subset constitute related receptor-negative subgroups characterized by low expression of GATA3-regulated genes and of genes responsible for cell-cell adhesion with enrichment for markers linked to stem cell function and epithelial-to-mesenchymal transition (EMT). In contrast to other breast cancers, claudin-low tumors and most MBCs showed a significant similarity to a "tumorigenic" signature defined using CD44(+)/CD24(-) breast tumor-initiating stem cell-like cells. MBCs and claudin-low tumors are thus enriched in EMT and stem cell-like features, and may arise from an earlier, more chemoresistant breast epithelial precursor than basal-like or luminal cancers. PIK3CA mutations, EMT, and stem cell-like characteristics likely contribute to the poor outcomes of MBC and suggest novel therapeutic targets. Comparison of reference samples against treatment

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BORG-dependent alterations in the transcriptome of D2.OR cells

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