Tan Xiaodong, Egami Hiroshi, Kamohara Hidenobu, Ishikawa Shinji, Kurizaki Takashi, Yoshida Naoya, Tamori Yasuhiko, Takai Eiji, Hirota Masahiko, Ogawa Michio
Department of Surgery II, Kumamoto University Medical School, Kumamoto, Japan.
Int J Oncol. 2004 Jan;24(1):65-73.
In our previous investigation, mitogen-activated protein kinase kinase 2 (MEK2) was detected as a factor which was correlated to the potential of invasion-metastasis. In this study, the immunocytochemical, immunohistochemical and mRNA expressions of MEK2 were examined in pancreatic cancer cell lines and tissue samples, respectively. Constitutive expressions of MEK2 and phosphorylated MEK (p-MEK) were observed in PC-1.0 and ASPC-1 cells, which exhibited a growth pattern of single cells, whereas the relevant expressions were quite faint in PC-1 cells and CAPAN-2 cells, which exhibited a growth pattern of island-like clonies. Simultaneous inductions of MEK2 expressions and cell dissociation were observed after the treatment with a conditioned medium (CM) of PC-1.0 cells. The expression of MEK2 and p-MEK were reduced and the cell aggregation was found in PC-1.0 and ASPC-1 cells after U0126 (a MEK inhibitor) treatment. In vivo, both the MEK2 and p-MEK overexpressed in human pancreatic cancer tissues and p-MEK was found to be more strongly expressed in the invasive front than that in the center of tumor (P<0.05). MEK2 is closely related to pancreatic cancer cell dissociation. MEK2 activation is probably involved in the first step of the cascade in the invasion-metastasis of pancreatic cancer.
在我们之前的研究中，丝裂原活化蛋白激酶激酶2（MEK2）被检测为与侵袭转移潜能相关的一个因子。在本研究中，分别检测了MEK2在胰腺癌细胞系和组织样本中的免疫细胞化学、免疫组织化学及mRNA表达。在呈单细胞生长模式的PC-1.0和ASPC-1细胞中观察到MEK2和磷酸化MEK（p-MEK）的组成性表达，而在呈岛状克隆生长模式的PC-1细胞和CAPAN-2细胞中，相关表达相当微弱。在用PC-1.0细胞的条件培养基（CM）处理后，观察到MEK2表达和细胞解离的同时诱导。在U0126（一种MEK抑制剂）处理后，PC-1.0和ASPC-1细胞中MEK2和p-MEK的表达降低，且发现细胞聚集。在体内，MEK2和p-MEK在人胰腺癌组织中均过表达，且发现p-MEK在肿瘤侵袭前沿的表达比肿瘤中心更强（P<0.05）。MEK2与胰腺癌细胞解离密切相关。MEK2激活可能参与胰腺癌侵袭转移级联反应的第一步。
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