Genomic and transcriptomic profiling of whole-genome-doubled triple-negative breast cancer cell populations

To investigate whether the mechanism of whole-genome doubling (WGD) results in distinct genomic and transcriptomic phenotypes, we compared three routes to WGD against their respective parental aneuploid controls across two triple-negative breast cancer (TNBC) cell lines (HCC1806 and MDA-MB-231). WGD mechanisms included naturally occurring cell-cell fusion and two drug-induced cell-cycle error mechanisms: mitotic slippage (MS) and cytokinesis failure (CF). All populations were profiled in biological triplicate by TagSeq (3' tag-based RNA-seq) for transcriptomic analysis and low-pass whole-genome sequencing (WGS) for copy-number profiling.