Abstract
The Notch pathway has two general regulatory mechanisms: its canonical pathway and the non-canonical pathway. The non-canonical Notch pathway is known that acts independently of its transcriptional factor to activate its target genes which do not belong to the HER, HES and HERP gene family, and has been linked to oncogenic processes and immune cell activation. Here we report the behavior of triple-negative breast cancer cells that maintain high activity of the non-canonical Notch pathway at the presence of ReNeg-AID a peptide which seems to be provoking both a change in the phenotype of the triple-negative breast cancer cells from epithelial cell to non-functional mesenchymal cell, as well as a cell's attempt to regain canonical Notch pathway activity. Finally, overexpression of the ReNeg-AID peptide in the triple-negative breast cancer cell line promoted a negative regulation of its transcriptional factor, intensifying the non-canonical Notch pathway activity and causing an oscillation or combination between the activities of the canonical and non-canonical mechanisms of Notch pathway due to the activation of Notch-1 and 3 receptors and the repression of Notch-2 and 4. Added to this must be the interactions that exist between Notch pathway with other signaling pathways that may also be in a state of deregulation in the cancer microenvironment.