Mutations in GNA11 induced spontaneously metastasizing tumors in a mouse model and activated the mitogen-activated protein kinase pathway.
在小鼠模型中，GNA11突变诱导了自发转移性肿瘤，激活了丝裂原活化蛋白激酶途径。
To investigate the change of mitogen activated protein kinase(MAPK) signaling pathway during prostate cancer progression, and therefore to explore its role on cell proliferation.
目的：研究前列腺癌进展中细胞丝裂原活化蛋白激酶（MAPK）信号通路的变化，探讨阻断此通路对前列腺癌细胞增殖的影响。
Mitogen-activated protein kinase pathway may closely associated with cell growth, differentiation and apoptosis, it may play an important role in cell death.
促有丝分裂原活化蛋白激酶（MAPK）信号传导途径与细胞生长、分化、凋亡等密切相关，在介导细胞凋亡过程中起着重要作用。
Mitogen-activated protein kinase pathway may closely associated with cell growth, differentiation and apoptosis, it may play an important role in cell death.
促有丝分裂原活化蛋白激酶（MAPK）信号传导途径与细胞生长、分化、凋亡等密切相关，在介导细胞凋亡过程中起着重要作用。
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