p38MAPK通路在佛波酯诱导人绒癌JAR细胞体外侵袭中的作用

目的 研究细胞内p38MAPK信号传导通路在人绒癌JAR细胞体外侵袭中的作用。方法 用ELISA法测定JAR细胞中p38MAPK的活性变化；用Tramwell细胞侵入系统检测细胞的侵袭作用；用MTT法评价细胞生长状况。结果 佛波酯(PMA)呈浓度依赖性地激活JAR细胞中p38MAPK。PMA能促进人绒癌JAR细胞的体外侵袭作用，而p38特异性抑制剂SB203580抑制了JAR细胞的侵袭能力。结论 p38MAPK通路在人滋养细胞的侵袭行为以及人绒癌的形成中具有重要作用。p38MAPK抑制剂可能会为人绒癌的防治提供新的途径。

Role of p38 pathway in PMA-induced in vitro invasion of JAR human choriocarcinoma cell line]

OBJECTIVE: To investigate the role of p38 mitogen-activated protein kinase (MAPK) signal transduction pathways in regulating the in vitro invasion of JAR human choriocarcinoma cells induced by phorbol 12-myristate 13-acetate (PMA). METHODS: ELISA was used to detect the kinase activity of the JAR cells in response to PMA stimulation, and the in vitro invasion capabilities of the stimulated cells were observed using transwell assay. Changes in the proliferation and activity of the JAR cells cultured in vitro following PMA treatment were also observed by MTT assay. RESULTS: p38 MAPK was activated dose-dependently in JAR cells upon the stimulation by PMA, which significantly enhanced the in vitro invasion of the JAR cells, while treatment of the cells with SB203580, a specific inhibitor of p38 MAPK, inhibited the invasion of the cells. The growth of the cells, as observed from the growth curves, was not affected by the treatment of PMA and/or SB203580. CONCLUSION: Activation of p38 MAPK signal transduction pathway may enhance the invasion capability of JAR cells, and p38 MAPK inhibition may therefore yield new possibility to control the invasion of choriocarcinoma.