Fine-tuning metabolic rewiring and translational machinery adaptation during an epithelial-mesenchymal transition in breast cancer cells.

During breast cancer progression, the epithelial to mesenchymal transition has been associated with metastasis and endocrine therapy resistance; however, the underlying mechanisms remain elusive. To gain insight into this process, we studied the transition undergone by MCF7-derived cells, which is driven by the constitutive nuclear expression of a MKL1 variant devoid of the actin binding domain (MKL1 ?N200). To identify major adaptive changes in gene expression during the luminal to basal-like transition, we carried out differential expression studies at both transcription and translation levels by RNA-Seq and ribosome profiling.