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.

The chromatin regulator WDR5 is a regulator of translation, and small molecule inhibitors or degraders of WDR5 can be used to treat triple-negative breast cancer.

Weakly migratory cancer cells facilitate their own escape from the primary tumor by releasing microvesicles that activate fibroblasts to remodel matrix and facilitate cancer cell metastasis.

HOTAIR is required in an ongoing manner when it regulates epigenetic status and reprograms cancer cell gene expression in promoting breast cancer metastasis.

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.

Metastases-associated fibroblasts show stage-dependent transcriptional plasticity and their rewiring is regulated by Myc.

Many extracellular matrix proteins that are up-regulated during breast tumor progression enhance metastasis, and some are prognostic indicators of poor survival.

RBM7 functions as a novel regulator of MFGE8 alternative splicing and p65 phosphorylation to counteract the metastatic potential of breast cancer, offering novel mechanistic insights into how abnormal splicing contributes to tumor aggressiveness.

Cellular acidity, capacity for net acid extrusion, and expression of acid-base transporters in human breast carcinomas independently predict variation in proliferative activity, lymph node metastasis, and patient survival.

CD44^-/CD24^- breast cancer cells contribute to delayed postoperative distant metastasis by their spontaneous conversion into CD44⁺/CD24^- breast cancer stem cells (CSCs).