We have identified a novel p53 pro-survival signaling pathway involving up-regulation/activation of a p53 target gene DDR1 and its down-stream signaling, which can influence the balance between cell death and survival in a p53 dependent response. Unlike other p53 target genes that function as either cell cycle inhibitors or apoptosis-promoters, DDR1 kinase promotes cell survival by counteracting p53-mediated cell death/apoptosis. Furthermore, accumulating evidence suggest that aberrant signaling through DDR1 kinase is closely associated with various steps of tumorigenesis and carcinogenesis, although little is known about the molecular mechanism(s) underlying the role of DDR1 in cancer. We have identified Comp #7 as a DDR1 tyrosine kinase inhibitor via the target-based small molecule array screening. Comp #7 specifically targets DDR1 kinase and its novel targets involved in EMT (Epithelial-Mesenchymal transition) pathway such as Slug, AKT and vimentin, which is known to play a major role in tumor progression and metastasis development. In addition, Comp #7 suppressed the activation of AKT prosurvival protein and of essential EMT pathway proteins involved in tumor migration/invasion. DDR1 kinase is highly expressed in a variety of human cancer and occasionally mutated in lung cancer and leukemia. Comp #7 binds directly to C-terminal part (intercellular region of the receptor) of DDR1 protein and specifically inhibits DDR1 kinase activation in response to its ligand. Comp #7  demonstrated antiproliferative activity against a range of DDR1-overexpressing cancer cell lines without high cytotoxicity in normal cells. Comp #7 also exhibited the potent anti-growth properties even in EGFR targeted (erlotinib and gefitinib) drug-resistant cancer cells. Comp #7 potently inhibited spontaneous formed breast cancer tumors and their associated metastasis in mice with no apparent adverse effects on normal organs. More particularly, the invention features a novel use of Comp #7 for effective treatment of the variety human cancers by inhibiting tumor migration/invasion via the inactivation of EMT pathway.