BACKGROUND: This study investigated the effects and mechanism of imatinib in inhibiting colon cancer cell proliferation.

MATERIAL AND METHODS: The SW480 cells were divided into 4 imatinib-treated groups: 0 μM, 1.25 μM, 2.5 μM, and 5μM. We analyzed the apoptosis and cell cycle of the 4 groups. The gene and protein expressions of p21, p27, HGF, and GAPDH were measured by RT-PCR and Western blot.

RESULTS: Compared with the 0-μM imatinib-treated group, the apoptosis of 1.25-μM, 2.5-μM, and 5.0-μM treated groups was significantly induced (P<0.05, all). The G1 phase was significantly up-regulated in the 1.25-μM, 2.5-μM, and 5.0-μM treated groups compared with the 0-μM imatinib-treated group (P<0.05, respectively), but the S and G2 phase of 3 imatinib-treated groups were significantly down-regulated (P<0.05, all). The gene and protein expressions of p27 and HGF were significantly different among the 4 groups (P<0.05, all).

CONCLUSIONS: Imatinib inhibits proliferation of colon cancer cells by reducing HGF and increasing p27 in a dose-dependent manner.

Keywords: Antineoplastic Agents - pharmacology, Cell Cycle - drug effects, Cell Proliferation - drug effects, Colonic Neoplasms - pathology, Cyclin-Dependent Kinase Inhibitor p21 - genetics, Dose-Response Relationship, Drug, Down-Regulation - drug effects, G1 Phase - drug effects, Glyceraldehyde-3-Phosphate Dehydrogenase (NADP+)(Phosphorylating) - genetics, Hepatocyte Growth Factor - genetics, Imatinib Mesylate - pharmacology, Proliferating Cell Nuclear Antigen - genetics, Protein Kinase Inhibitors - pharmacology, Random Allocation