ITGB4 is overexpressed in HCC tissues and aggressive HCC cells and associated with HCC metastases.
The ITGB4–EGFR unit promotes anchorage independence by activating AKT signaling pathway.
The ITGB4–EGFR unit triggers the FAK rather than SRC to activate AKT pathway.
ITGB4 enhances tumor growth and pulmonary metastases of HCC in vivo.