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Figure 1. Interconnection between EMT and immune checkpoint based immunotherapy. The diagram illustrates the transition of epithelial-like tumor cells toward a mesenchymal phenotype is associated with immune checkpoint regulation. EMT is induced by several factors including cytokines, upregulation of transcription factors and immune checkpoint molecule PD-L1. EMT is accompanied by the modulation of well-known EMT markers, the loss of epithelial marker E-cadherin and gain of mesenchymal marker Vimentin. Mesenchymal-like tumor cells with elevated expression of different immune checkpoint molecules are more resistant to ICI therapy compared with epithelial-like tumors. The coexistence of features of EMT and expression of immune checkpoint molecules opens the possibility of a mechanistic link between these processes and EMT markers in combination with immune checkpoint molecules can be studied in a prognostic or therapeutic context. PD-L1: programmed death protein ligand -1; EMT: epithelial-to-mesenchymal transition