Fig. 8

A schematic model visualizing of cholesterol-IKBKB/FOXO3a/KRT14 axis in promoting metastasis of TNBC and the mechanism of ADV-ApoA1 in inhibiting metastasis of TNBC. In cholesterol-IKBKB/FOXO3a/KRT14 axis, KRT14 acts as a critical regulator of TNBC invasion and metastasis, while FOXO3a functions as a transcription repressor of KRT14. ApoA1-mediated cholesterol efflux effectively reduces the phosphorylation of FOXO3a by IKBKB, which leads to the nuclear translocation of FOXO3a and consequently suppresses KRT14 transcription and lung metastasis in TNBC. Replicative ADV-ApoA1 with E1A protein upregulates ABCA1, facilitating ApoA1-mediated cholesterol efflux