Fig. 7

Graphic abstract of molecular mechanisms of MED1 promoting tumor progression in OSCC. A For untreated metastatic OSCC cells, MED1 facilitates MMP9 expression by promoting the transcription of MMP9, resulting in heightened migration and invasion of metastatic OSCC cells, just like strengthen the destructive force of "bandits". Additionally, MED1 upregulates PD-L1 expression via activation of the Notch signaling pathway, resulting in diminished cytotoxicity of CD8⁺ T cells within the tumor microenvironment and consequent attenuation of anti-tumor immunity responses. This behavior is similar to weaken the fighting capacity of "police". B For MED1 knockdown metastatic OSCC cells, the transcription of MMP9 is inhibited, leading to decreased migration and invasion of metastatic OSCC cells, just like weaken the destructive force of "bandits". This inhibition also leads to a decrease in PD-L1 expression through the suppression of Notch signaling pathway, indirectly enhancing the cytotoxic activity of CD8⁺ T cells in the TME and strengthening antitumor immunity responses. This behavior is similar to strengthen the fighting capacity of "police". MMP9: matrix metallopeptidase 9, POL II: RNA polymerase II, TATA: TATA box, PD-L1: programmed cell death ligand 1, NICD: Notch intracellular domain, PD-1: programmed cell death 1, IFN-γ: interferon-γ, IL-2: Interleukin-2