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通过β-连环蛋白免疫组织化学染色评估炎症诱导的大鼠结肠癌发生过程中异常隐窝病灶的恶性潜能。

Evaluation of the malignant potential of aberrant crypt foci by immunohistochemical staining for beta-catenin in inflammation-induced rat colon carcinogenesis.

作者信息

Furihata Tadashi, Kawamata Hitoshi, Kubota Keiichi, Fujimori Takahiro

机构信息

Department of Gastroenterological Surgery, Dokkyo University School of Medicine, 880 Kitakobayashi, Mibu, Shimotsuga, Tochigi 321-0293, Japan.

出版信息

Int J Mol Med. 2002 Apr;9(4):353-8.

Abstract

We previously showed that colitis enhanced the development of cancer and aberrant crypt foci (ACF) in 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in Fischer 344 rats. In this study, we examined the effect of two different anti-inflammatory drugs [non-steroidal anti-inflammatory drugs (NSAIDs: Fenbufen) and a platelet activating factor-receptor antagonist (PAF-RA)] on the inflammation-induced rat colon carcinogenesis. Furthermore, we examined the expression and the localization of beta-catenin protein, and the proliferating cell nuclear antigen (PCNA)-labeling index (LI) in ACF and cancer. PAF-RA significantly decreased the incidence of ACF in the rats (p<0.05), but Fenbufen did not affect the incidence of ACF and cancer. In most of the ACF (91%), beta-catenin was localized at the cell membrane like in normal colon epithelium. In about 9% of the ACF, beta-catenin was overexpressed not only on the cell membrane but also in the cytoplasm. In all of the cancer cells, beta-catenin was overexpressed in the nucleus. When we compared the PCNA-LI in the ACF showing normal beta-catenin expression pattern with that in the ACF showing abnormal beta-catenin expression pattern (overexpression in cytoplasm), there was no significant difference of the PCNA-LI in these two different types of ACF. These findings suggest that immunohistochemical staining of ACF for beta-catenin can evaluate the malignant potential of ACF, and that PAF-RA can be used for preventing the development of ACF in inflammation-induced carcinogenesis.

摘要

我们之前的研究表明,在费希尔344大鼠中,结肠炎会增强1,2 - 二甲基肼(DMH)诱导的结肠癌发生及异常隐窝病灶(ACF)的发展。在本研究中,我们检测了两种不同抗炎药物[非甾体抗炎药(NSAIDs:芬布芬)和血小板活化因子受体拮抗剂(PAF - RA)]对炎症诱导的大鼠结肠癌发生的影响。此外,我们检测了β - 连环蛋白的表达及定位,以及ACF和癌组织中增殖细胞核抗原(PCNA)标记指数(LI)。PAF - RA显著降低了大鼠ACF的发生率(p<0.05),但芬布芬对ACF和癌的发生率没有影响。在大多数ACF(91%)中,β - 连环蛋白像在正常结肠上皮中一样定位于细胞膜。在约9%的ACF中,β - 连环蛋白不仅在细胞膜上过度表达,还在细胞质中过度表达。在所有癌细胞中,β - 连环蛋白在细胞核中过度表达。当我们比较β - 连环蛋白表达模式正常的ACF与β - 连环蛋白表达模式异常(细胞质中过度表达)的ACF中的PCNA - LI时,这两种不同类型的ACF中的PCNA - LI没有显著差异。这些发现表明,对ACF进行β - 连环蛋白的免疫组化染色可以评估ACF的恶性潜能,并且PAF - RA可用于预防炎症诱导的癌变中ACF的发展。

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