An integrin beta4-EGFR unit promotes hepatocellular carcinoma lung metastases by enhancing anchorage independence through activation of FAK-AKT pathway
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ITGB4 is overexpressed in HCC tissues and aggressive HCC cells and associated with HCC metastases.

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The ITGB4–EGFR unit promotes anchorage independence by activating AKT signaling pathway.

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The ITGB4–EGFR unit triggers the FAK rather than SRC to activate AKT pathway.

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ITGB4 enhances tumor growth and pulmonary metastases of HCC in vivo.

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