ADAM9 overexpression enhances cell adhesion and invasion of non-small cell lung cancer cells via modulation of other adhesion molecules and changes in sensitivity to growth factors, thereby promoting metastatic capacity to the brain.

ADAM9 up-regulates N-cadherin via miR-218 suppression in lung adenocarcinoma cells.

ADAM9 high expression is correlated positively and significantly with HDGF high expression in non-small cell lung cancer.

Results show how ADAM9 regulates lung cancer metastasis to the brain by facilitating the tPA-mediated cleavage of CDCP1.

ADAM9 silencing inhibits the tumor growth of non-small lung cancer in vitro and in vivo.

ADAM9 enhances CDCP1 protein expression by suppressing miR-218 for lung tumor metastasis

These results revealed that ADAM9 down-regulates miR-1 via activating EGFR signaling pathways, which in turn enhances CDCP1 expression to promote lung cancer progression.

hese results emphasize the critical influence of ADAM9 on lung cancer progression and aggressiveness. ADAM9 should at least be a marker of cancer aggressiveness and a potential therapeutic target for cancer treatment.