Expression of 11β-hydroxysteroid dehydrogenase type 2 is deregulated in colon carcinoma
Language English Country Spain Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
24189979
DOI
10.14670/hh-29.10.489
PII: HH-11-406
Knihovny.cz E-resources
- MeSH
- 11-beta-Hydroxysteroid Dehydrogenase Type 1 analysis biosynthesis MeSH
- 11-beta-Hydroxysteroid Dehydrogenase Type 2 analysis biosynthesis MeSH
- Adenocarcinoma enzymology MeSH
- Adenomatous Polyps enzymology MeSH
- Child MeSH
- Adult MeSH
- Down-Regulation MeSH
- Colorectal Neoplasms enzymology MeSH
- Real-Time Polymerase Chain Reaction MeSH
- Laser Capture Microdissection MeSH
- Middle Aged MeSH
- Humans MeSH
- Adolescent MeSH
- Young Adult MeSH
- Biomarkers, Tumor analysis MeSH
- Reverse Transcriptase Polymerase Chain Reaction MeSH
- Precancerous Conditions enzymology MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Transcriptome MeSH
- Check Tag
- Child MeSH
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Adolescent MeSH
- Young Adult MeSH
- Male MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- 11-beta-Hydroxysteroid Dehydrogenase Type 1 MeSH
- 11-beta-Hydroxysteroid Dehydrogenase Type 2 MeSH
- Biomarkers, Tumor MeSH
Although the effects of glucocorticoids on proliferation, differentiation and apoptosis are well known, and steroid hormones have been identified to play a role in pathogenesis and the development of various cancers, limited data are available regarding the relationship between the local metabolism of glucocorticoids and colorectal adenocarcinoma (CRC) formation. Glucocorticoid metabolism is determined by 11β-hydroxysteroid dehydrogenases type 1 and 2 (11HSD1, 11HSD2), which increase the local concentration of cortisol due to the reduction of cortisone, or decrease this concentration due to the oxidation of cortisol. The objective of this study was to evaluate the extent of 11HSD1 and 11HSD2 mRNA in pre-malignant colorectal polyps and in CRC. The specimens were retrieved from patients by endoscopic or surgical resection and the expression of 11HSD1 and 11HSD2 was measured by real-time PCR. The polyps were of the following histological types: hyperplastic polyps and adenomas with low- or high-grade dysplasia. The neoplastic tissue of CRC obtained during tumor surgery was also studied. It was found that 11HSD2 was not only downregulated in CRC but already in the early stages of neoplastic transformation (adenoma with low-grade dysplasia). In contrast, the level of 11HSD1 was significantly increased in CRC but not in pre-malignant polyps. The results demonstrate that the downregulation of 11HSD2 gene expression is a typical feature of the development of colorectal polypous lesions and their transformation into CRC.
2nd Department of Internal Medicine 3rd Faculty of Medicine Charles University Prague Czech Republic
Department of Pathology 3rd Faculty of Medicine Charles University Prague Czech Republic
Institute of Physiology Academy of Sciences of the Czech Republic Prague Czech Republic
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