NOTCH2 promotes EMT progression and M2-like TAM polarization in colorectal cancer

Through clinical database analysis, histological validation, and in vitro gain- and loss-of-function assays, we identified that NOTCH2 expression is significantly upregulated in CRC tissues and correlates with advanced clinical stages and poor patient prognosis.

Furthermore, functional and mechanistic studies revealed that NOTCH2 activation suppresses the epithelial marker E-cadherin while upregulating the mesenchymal marker Vimentin to accelerate EMT, subsequently inducing M2-like tumor-associated macrophage (TAM) polarization. These findings provide a novel molecular basis for NOTCH2 as a critical oncogenic driver and a potential therapeutic target for CRC.