Expression of sucrase and intestinal-type alkaline phosphatase in colorectal carcinoms in rats treated with methylazoxymethanol acetate

Abstract

In this study the small-intestine phenotype in rat colonic tumors was investigated in terms of sucrase and intestinal-type alkaline phosphatase (I-ALP) activity. F344 rats were given intraperitoneal injections of methylazoxymethanol acetate at a dose level of 25 mg/kg body weight once a week for 8 weeks and were killed 40 weeks after the first injection. Sucrase and I-ALP activities in proximal and distal colon adenocarcinomas were significantly higher than those in the normal colon epithelium. In the jejunum, by contrast, normal tissue had significantly higher levels than tumors. Immunohistochemical staining of I-ALP was also strong in striated cell borders of colon adenocarcinoma cells. These data suggest that, whereas absorptive cells of the small intestine lose their own traits with tumor development, colonocytes acquire phenotypic features of the small intestine. Intestinal enzymes associated with the striated-cell border, such as sucrase and I-ALP, may be useful markers for malignant phenotypic expression in colonocytes.

Duodenal brush border intestinal alkaline phosphatase activity affects bicarbonate secretion in rats

“…3K). Figure 3L depicts the longitudinal axis of ELF-based BBM AP activity (or apical membrane AP activity in the stomach), which was highest in the proximal and distal duodenum and declined in the jejunum, but low in the fundus, antrum, ileum, and colon, consistent with previous studies (13,29,55,68).…”

Cellular differentiation status of epithelial polyps of the colorectum: the gastric foveolar cell‐type in hyperplastic polyps

“…Yoshida et al. , 21 however, demonstrated small intestinal differentiation of colorectal adenocarcinomas induced by a chemical carcinogen in rats as well as in human tumours. Further investigation, using other small intestinal phenotypic markers, such as alkaline phosphatase, sucrase, or villin, seems to be needed.…”

The Promyelocytic Leukemia Zinc Finger (PLZF ) gene is a novel transcriptional target of the CCAAT‐Displacement‐Protein (CUX1) repressor

“…An interesting hypothesis is that intestinal disorders, such as colorectal cancer (CRC), could evolve from the subtle accumulation of genetic alterations in the transcriptome that leads to a divergence of these cells from their original identities [2]. Colorectal adenomas and carcinomas are often associated with phenotypic and genetic characteristics of the normal adult small intestinal epithelium [3–6]. During embryonic life, the colon passes through a transient developmental stage that reproduces the small intestinal phenotype with the expression of small intestinal‐specific genes, such as sucrase–isomaltase (SI) [7].…”

“…Because of the implication of Plzf in the regulation of stem cell maintenance, as well as Wnt and Ras signaling, in other systems, our observations suggest that the novel genetic relationship between CUX1 and PLZF could be of relevance to human diseases, such as leukemia, and open up a new field of investigation for the implication of these regulators during intestinal polyposis and cancer. normal adult small intestinal epithelium [3][4][5][6]. During embryonic life, the colon passes through a transient developmental stage that reproduces the small intestinal phenotype with the expression of small intestinalspecific genes, such as sucrase-isomaltase (SI) [7].…”