Inactivation of a multifunctional RNA-binding protein can lead to the acquisition of pro-metastatic phenotypes, possibly by stabilizing large-scale transcriptomic changes that provide a selective advantage during cancer progression.
Transcription elongation by the elongation factor P-TEFb promotes the epithelial–mesenchymal transition and metastasis of breast cancer cells, implicating inhibition of this factor as a potential treatment for the late stages of this cancer.
Loss of RUNX1, a key regulator of estrogen receptor-positive luminal breast cells, impairs mammary epithelial differentiation and contributes to luminal breast cancer via genetic interactions with a loss of p53 or RB1.
A combination of animal models reveal how the molecular mechanisms of exosome secretion (RalA/B-dependent) are linked to their cargo content and their function in breast cancer pre-metastatic niche formation.
Two common mutant versions of estrogen receptor alpha achieve constitutive activity and hormone-resistance by preferentially adopting a suite of conformations that expose the coregulator-binding surface.
Development and application of highly sensitive in situ transcriptomics method, Flura-seq, in identifying dynamic organ-specific transcriptomes in early stage breast cancer metastasis have been described.