Apoptosis, proliferation and p12doc-1 profiles in normal, dysplastic and malignant squamous epithelium of the Syrian hamster cheek pouch model
Apoptosis, proliferation and p12doc-1 profiles in normal, dysplastic and malignant squamous epithelium of the Syrian hamster cheek pouch model
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DOI：
10.1016/s1368-8375(01)00055-0
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发表时间：
2002-04-01
期刊：
影响因子：
4.8
通讯作者：
Todd, R
中科院分区：
文献类型：
--
作者：
Kohno, Y;Patel, V;Todd, R
增殖和凋亡之间动态平衡的破坏被广泛认为是导致人类口腔癌发生的原因之一。以叙利亚仓鼠口腔癌模型为研究对象，采用原位末端标记法、增殖细胞核抗原和p12(Doc-1)免疫组织化学方法分别检测正常、增生性、异型和恶性口腔上皮中角质形成细胞的凋亡率、增殖率和p12(Doc-1)的表达。TUNEL阳性细胞百分率从正常上皮逐渐增加到发育不良上皮(P<；0.0019)，但在恶性上皮中恢复到正常角质形成细胞水平(P<；0.0012)。角质形成细胞的总凋亡率与增殖率基本一致，直到异型上皮向恶性上皮过渡，比例明显降低(P<；0.008)，p12(Doc-1)标记显示相似的表达模式(P<；0.05)。这项研究表明，细胞凋亡、增殖和p12(DOC-1)的表达反映了人类口腔癌发生过程中已报道的变化，并支持使用叙利亚仓鼠模型进一步研究这些途径。(C)2002爱思唯尔科学有限公司。保留所有权利。
Disruption of the homeostatic balance between proliferation and apoptosis is widely believed to contribute to human oral carcinogenesis. Using the Syrian hamster oral cancer model, we examined normal, hyperplastic, dysplastic and malignant oral epithelium for the fraction of apoptotic, proliferating and p12(doc-1) expressing keratinocytes using the TUNEL assay, as well as PCNA and p12(doc-1) immunostaining, respectively. The percentage of TUNEL positive cells progressively increased from normal to dysplastic epithelium (P < 0.0019), but returned to normal keratinocyte levels in the malignant epithelium (P < 0.0012). The overall ratio of apoptotic to proliferating keratinocytes remains similar until the transition between dysplastic and malignant epithelium, where the ratio is markedly reduced (P < 0.05), p12(doc-1) labeling demonstrated a similar expression pattern (P < 0.008). This study demonstrates that apoptosis, proliferation and the expression of p12(doc-1) reflects alterations reported during human oral carcinogenesis and supports the use of the Syrian hamster model for the further examination of these pathways. (C) 2002 Elsevier Science Ltd. All rights reserved.