Cyclooxygenase (COX)-2 immunoreactivity and relationship to p53 and Ki-67 expression in colorectal cancer
Cyclooxygenase (COX)-2 immunoreactivity and relationship to p53 and Ki-67 expression in colorectal cancer
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DOI：
10.1007/s005350050242
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发表时间：
1999-04-01
影响因子：
6.3
通讯作者：
Terano, A
中科院分区：
文献类型：
--
作者：
Sakuma, K;Fujimori, T;Terano, A
非甾体类抗炎药（NSAID）的肿瘤抑制作用被认为是由于环氧合酶（COX）-2活性降低所致，尽管COX-2在结肠粘膜和结直肠癌中的作用尚未确定，但癌症中的Ki-67免疫反应性也引起了人们的关注，因为Ki-67反映了细胞增殖，而p53免疫反应性也令人感兴趣，因为它反映了结直肠病变的恶性程度。因此，为了确定这些相关性，我们研究了散发性和溃疡性结肠炎 (UC) 相关结直肠癌患者的癌性和非癌性组织中 COX-2、p53 和 Ki-67 表达的分布和强度。我们从 21 名患者中选择了 21 份结直肠癌标本，这些标本是通过手术切除或结肠镜活检获得的，其中包括 3 名 UC 患者（13 名男性和 8 名女性；年龄 42-78 岁）。苏木精和伊红染色标本的组织学检查显示，9 个分化良好； 11、中等分化； 1为低分化腺癌。我们使用抗COX-2、p53和Ki-67抗血清，通过标记的链霉亲和素生物素法进行免疫组织化学染色，然后对染色强度和分布进行评估和分级。癌组织中的 COX-2 染色比非癌组织中的染色更强烈。与 UC 相关的结直肠癌染色不强烈。 COX-2、p53和Ki-67的阳性率分别为38.1%、38.1%和47.6%。 COX-2、p53 和 Ki-67 表达的分布或强度之间没有关系。我们的结果表明结直肠癌组织过度表达COX-2，但COX-2、p53和Ki-67表达之间没有关系，表明COX-2表达可能与细胞增殖或恶性程度无关。然而，有必要确定癌组织中的COX-2是否参与了癌变过程，或者仅仅是癌症的产物。
The tumor-suppressive effects of nonsteroidal antiinflammatory drugs (NSAIDs) have been suggested to be due to a reduction in cyclooxygenase (COX)-2 activity, although the effects of COX-2 in the colonic mucosa and in colorectal cancer have not been determined, Ki-67 immunoreactivity in cancers is also attracting attention, as Ki-67 reflects cell proliferation, while p53 immunoreactivity is also of interest, as it reflects the malignancy of colorectal lesions. Accordingly, to determine these correlation, we investigated the distribution and intensity of COX-2, p53 and Ki-67 expression in both cancerous and non-cancerous tissues from patients with sporadic and ulcerative colitis (UC)associated colorectal cancer. We selected 21 colorectal cancer specimens, obtained by surgical resection or colonoscopic biopsy, from 21 patients, including 3 with UC (13 men and 8 women; aged 42-78 years). Histological examination of hematoxylin and eosin-stained specimens revealed that 9 were well differentiated; 11, moderately differentiated; and 1 was a poorly differentiated adenocarcinoma. We used anti-COX-2, p53, and Ki-67 antisera to perform immunohistochemical staining by the labelled streptavidin biotin method and then assessed and graded the staining intensity and distribution. COX-2 staining was more intense in cancer tissue than in non-cancerous areas. Colorectal cancers associated with UC were not stained intensely. COX-2, p53, and Ki-67 positivity rates in were 38.1%, 38.1%, and 47.6%,respectively. There were no relationships among the distributions or intensities of COX-2, p53, and Ki-67 expression. Our results indicate that colorectal cancer tissues overexpress COX-2, but that there are no relationships between COX-2, p53, and Ki-67 expression, suggesting that COX-2 expression may not be related to cell proliferation or to the grade of malignancy. However, it is necessary to determine whether COX-2 in cancer tissue is involved in carcinogenesis or whether it is simply a product of cancer.