中期因子通过丝裂原活化蛋白激酶（MAPK）和蛋白激酶B（Akt）信号通路诱导成釉细胞瘤生长。
Midkine induced growth of ameloblastoma through MAPK and Akt pathways.
作者信息
Sandra F, Harada H, Nakamura N, Ohishi M
机构信息
Laboratory of Oral Cellular and Molecular Biology, Faculty of Dental Science, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
出版信息
Oral Oncol. 2004 Mar;40(3):274-80. doi: 10.1016/j.oraloncology.2003.08.011.
Midkine (MK) is expressed during tooth development and, since ameloblastoma is thought to be arisen from the epithelium of the odontogenic apparatus or its remnant tissues, the effect of MK in ameloblastoma cell growth should be examined. The expression and function of MK were examined using 37 ameloblastoma tissues and AM-1 cells, an HPV-16DNA transfected ameloblastoma cell line. We found that MK was immunohistochemically expressed in 70% of ameloblastoma cases and AM-1 cells. By stimulation with 100 ng/ml MK, the growth of AM-1 cells was accelerated two fold by the 9th day. MK could induce phosphorylation of p44/42 MAPK (Thr202/Tyr204) and Akt (Ser473 and Thr308), and by pretreatment of PD98059, MEK1 inhibitor, or LY294002, PI3K inhibitor, MK-stimulated-phosphorylation of MAPK and Akt and MK-stimulated growth of AM-1 cells were inhibited. These results suggested that MK induced growth of ameloblastoma is through the MAPK and Akt pathways.
中期因子（MK）在牙齿发育过程中表达，由于成釉细胞瘤被认为起源于牙源性器官的上皮或其残余组织，因此应研究MK在成釉细胞瘤细胞生长中的作用。使用37例成釉细胞瘤组织和AM-1细胞（一种HPV-16DNA转染的成釉细胞瘤细胞系）检测了MK的表达和功能。我们发现，70%的成釉细胞瘤病例和AM-1细胞中MK呈免疫组化表达。通过用100 ng/ml MK刺激，到第9天时AM-1细胞的生长加速了两倍。MK可诱导p44/42丝裂原活化蛋白激酶（Thr202/Tyr204）和Akt（Ser473和Thr308）磷酸化，并且通过用MEK1抑制剂PD98059或PI3K抑制剂LY294002预处理，MK刺激的丝裂原活化蛋白激酶和Akt磷酸化以及MK刺激的AM-1细胞生长受到抑制。这些结果表明，MK诱导成釉细胞瘤生长是通过丝裂原活化蛋白激酶和Akt途径。
Zotero 插件