Fig. 8: Schematic model of the mechanism by which HORMAD1 functions to promote the malignant phenotypes of lung cancer cells.

Aberrant HORMAD1 expression suppresses the degradation of cytosolic β-catenin and promotes nuclear β-catenin accumulation by regulating AKT/GSK-3β signaling to activate the Wnt/β-catenin pathway, accompanied with upregulation of downstream target genes and induction of EMT to promote tumor growth and metastasis in lung cancer.