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Midkine (MK), a heparin binding growth factor is expressed during the tooth development. Since ameloblastoma is thought to arise from the epithelium of the odontogenic apparatus, or its remnant tissues, the affect of MK in ameloblastoma cell growth is necessary to be examined. MK was immunohistochemically expressed in the 49% of ameloblastoma cases. Various concentrations of MK was applied to AM-1 cells, HPV-16DNA transfected ameloblastoma cell line. The growth of 100 ng/ml MK-stimulated AM-1 cells was two folds higher on the 9th day than that of the untreated one. MK induced the signal of phospho-p44/42 MAPK (Thr202/Tyr204) and phospho-Akt (Ser473 and Thr308) in the time dependent manner. PD98059, MEK1 inhibitor, or LY294002, PI3K inhibitor had the affect to inhibit the MK-stimulated-MAPK or -Akt pathways respectively, which was started in 5 min after MK stimulation. Furthermore, the pretreatment of PD98059 or LY294002 to the AM-1 cells, vanished the MK-stimulated high cell growth. These results suggested MK was playing a role in the growth of ameloblastoma through the MAPK and Akt pathway. |
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