Fig. 7

Schematic diagram depicts the function that LATS1/2 upregulates MHC-I expression through positively modulating the IFN-γ-STAT1-IRF1 signaling. LATS1/2 directly interact with and phosphorylate STAT1 at Ser727, a crucial transcription factor for MHC-I upregulation in response to interferon-gamma (IFN-γ) signaling, to promote STAT1 accumulating and moving into the nucleus to enhance the transcriptional activation of IRF1/NLRC5 on MHC-I. The dysregulation of LATS1/2 in EC leads to immune evasion through the down-regulation of MHC-I, which may result in primary and acquired resistance to immune checkpoint blockade therapy