Kumamoto H, Ooya K
Department of Oral Medicine and Surgery, Tohoku University Graduate School of Dentistry, Sendai, Japan.
J Oral Pathol Med. 2007 Oct;36(9):543-9. doi: 10.1111/j.1600-0714.2007.00555.x.
To evaluate roles of mitogen-activated protein kinases (MAPKs) in oncogenesis and cytodifferentiation of odontogenic tumors, expression of phosphorylated JNK (p-JNK), p38 MAPK (p-p38 MAPK), and ERK5 (p-ERK5) was analyzed in ameloblastic tumors as well as in tooth germs.
Ten tooth germs, 47 ameloblastomas, and 5 malignant ameloblastic tumors were examined immunohistochemically with the antibodies against p-JNK, p-p38 MAPK, and p-ERK5.
Immunoreactivity for p-JNK was detected in epithelial or neoplastic cells detached from the basement membrane in 7 tooth germs and 7 ameloblastomas, and the expression levels of p-JNK in ameloblastic tumors were significantly lower than that in tooth germs. Expression of p-p38 MAPK was found in epithelial or neoplastic cells in tooth germs and ameloblastic tumors except for two ameloblastomas, and increased expression was found in keratinizing cells of acanthomatous ameloblastomas. The expression level of p-p38 MAPK in ameloblastomas was significantly higher than the levels in tooth germs and malignant ameloblastic tumors. Immunoreactivity for p-ERK5 was found predominantly in epithelial or neoplastic cells near the basement membrane in tooth germs and ameloblastic tumors. The expression levels of p-ERK5 in ameloblastic tumors were slightly higher than that in tooth germs, and plexiform ameloblastomas showed significantly higher p-ERK5 expression than follicular ameloblastomas.
Expression of p-JNK, p-p38 MAPK, and p-ERK5 in tooth germs and ameloblastic tumors suggests that these MAPK signaling pathways contribute to cell proliferation, differentiation, or apoptosis in both normal and neoplastic odontogenic tissues. Altered expression of these phosphorylated MAPKs in ameloblastic tumors may be involved in oncogenesis and tumor cell differentiation.
为评估丝裂原活化蛋白激酶（MAPKs）在牙源性肿瘤的发生和细胞分化中的作用，分析了磷酸化JNK（p-JNK）、p38 MAPK（p-p38 MAPK）和ERK5（p-ERK5）在成釉细胞瘤以及牙胚中的表达情况。
采用抗p-JNK、p-p38 MAPK和p-ERK5的抗体，对10个牙胚、47例成釉细胞瘤和5例恶性成釉细胞瘤进行免疫组织化学检测。
在7个牙胚和7例成釉细胞瘤中，从基底膜脱离的上皮或肿瘤细胞中检测到p-JNK的免疫反应性，成釉细胞瘤中p-JNK的表达水平明显低于牙胚。除2例成釉细胞瘤外，在牙胚和成釉细胞瘤的上皮或肿瘤细胞中发现了p-p38 MAPK的表达，在棘皮瘤型成釉细胞瘤的角化细胞中发现表达增加。成釉细胞瘤中p-p38 MAPK的表达水平明显高于牙胚和恶性成釉细胞瘤。在牙胚和成釉细胞瘤中，p-ERK5的免疫反应性主要见于基底膜附近的上皮或肿瘤细胞。成釉细胞瘤中p-ERK5的表达水平略高于牙胚，丛状成釉细胞瘤的p-ERK5表达明显高于滤泡型成釉细胞瘤。
p-JNK、p-p38 MAPK和p-ERK5在牙胚和成釉细胞瘤中的表达表明，这些MAPK信号通路在正常和肿瘤性牙源性组织的细胞增殖、分化或凋亡中发挥作用。成釉细胞瘤中这些磷酸化MAPKs的表达改变可能与肿瘤发生和肿瘤细胞分化有关。
