title: Effects and Mechanism of Imatinib in Inhibiting Colon Cancer Cell Proliferation.
abstract: 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.
authors: Department of Elderly Digestion, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China (mainland).
authors: Lv
authors: L
authors: Samei
authors: Department of Elderly Digestion, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China (mainland).
authors: Pang
authors: P
authors: Yaling
authors: Department of Ophthalmology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China (mainland).
authors: Yang
authors: Y
authors: Lihua
authors: Department of Endocrinology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China (mainland).
authors: Zhang
authors: Z
authors: Yan
authors: Department of Endocrinology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China (mainland).
authors: Jiang
authors: J
authors: Shuyan
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D002453:Cell Cycle / Q000187:drug effects; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D003110:Colonic Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000096:biosynthesis / Q000235:genetics; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation / Q000187:drug effects; D016193:G1 Phase / Q000187:drug effects; D024602:Glyceraldehyde-3-Phosphate Dehydrogenase (NADP+)(Phosphorylating) / Q000096:biosynthesis / Q000235:genetics; D017228:Hepatocyte Growth Factor / Q000096:biosynthesis / Q000235:genetics; D006801:Humans; D000068877:Imatinib Mesylate / Q000494:pharmacology*; D018809:Proliferating Cell Nuclear Antigen / Q000096:biosynthesis / Q000235:genetics; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D011897:Random Allocation
chemical_list: D000970:Antineoplastic Agents; C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; C066855:HGF protein, human; D018809:Proliferating Cell Nuclear Antigen; D047428:Protein Kinase Inhibitors; C413374:p27 antigen; D017228:Hepatocyte Growth Factor; D000068877:Imatinib Mesylate; D024602:Glyceraldehyde-3-Phosphate Dehydrogenase (NADP+)(Phosphorylating)