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Post-transcriptional regulation of Aurora Kinase A (AURKA) through alternative polyadenylation of its mRNA determines miRNA influence and is a feature of cell cycle-specific AURKA expression whose impairment leads to acquisition of cancer phenotypes.

Identification of a pro-tumorigenic and pro-metastatic role of EHD2 protein in triple-negative breast cancer (TNBC) through the store-operated calcium entry (SOCE) pathway provides a rationale for potential targeting of EHD2-overexpressing TNBC with SOCE inhibitors.

GDE3 is a transmembrane GPI-specific phospholipase C that sheds the urokinase receptor (uPAR) from the cell surface resulting in loss of uPAR function in breast cancer cells and reduced tumor growth.

Breast luminal epithelial cells are the hotspots of aging-associated changes, which prime aged epithelia for oncogenic gene activation and may explain individual differences in breast cancer susceptibility due to the aging-associated increase in gene expression variances in luminal epithelia.

SOX11+ breast tumours display reactivated embryonic developmental signalling and organogenetic features and are at elevated risk of developing metastases, so may benefit from more aggressive therapies.

3D culture of breast cancer in biologically relevant ECM potentiates the growth-inhibitory effects of unacylated ghrelin and AZP-531, and clinical response may be predictable based on a MAPK gene signature.

Genetic mouse models and human cell lines show that Musashi proteins promote an epithelial/luminal state and inhibit epithelial–mesenchymal transition (EMT), and genome-wide maps of translational regulatory targets connect Musashi proteins to an epithelial alternative splicing program and to the regulation of EMT.

Copy number alteration heterogeneity exists in many shapes and forms in breast cancer genomes and single-cell genomics is a powerful tool to further our understanding of its nature and significance.

A microfluidic device induces doxorubicin-resistant polyaneuploid cancer cells from triple negative breast cancer cells, revealing NUPR1/HDAC11 axis dysfunction drives chemoresistance, increasing tumor heterogeneity and impacting clinical outcomes.

PRMT7-mediated SHANK2 methylation regulates breast cancer metastasis by activating endosomal FAK signals, and may provide potential clues for tumour metastasis treatment strategies.