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.

Cells adapt to extracellular hypertonicities using regulatory volume increase (RVI), and TNFR1-mediated NFkB activation is indispensable for RVI, but the increased cytoplasmic macromolecular crowding can inhibit TNFR1 signaling and prevent RVI at severe hypertonicities.

eIF3, despite being a general translation initiation factor, functions in mRNA-specific regulation, having a profound impact on the synthesis and activation of the MAPK pathway components and ribosomal proteins.

Vangl2 induced by inflammation recruits ubiquitin ligase PDLIM2 and increases K63-linked ubiquitination on p65, which promotes the recognition of p65 by cargo receptor NDP52 and the autophagic degradation of p65.