Expression of Cold-Inducible RNA-Binding Protein in the Normal Endometrium, Endometrial Hyperplasia, and Endometrial Carcinoma
| Autor: | Jun Fujita, Takashi Kusakari, Masaki Mandai, Shingo Fujii, Ken Fukuhara, Kanako Nanbu, Atia A. Hamid, Masatoshi Kariya |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Adult
medicine.medical_specialty Pathology Stromal cell Blotting Western Biology Endometrium Pathology and Forensic Medicine Western blot Internal medicine medicine Humans Aged Neoplasm Staging medicine.diagnostic_test Binding protein RNA-Binding Proteins Obstetrics and Gynecology Middle Aged Cell cycle Hyperplasia medicine.disease Immunohistochemistry Endometrial Neoplasms Endometrial hyperplasia Ki-67 Antigen Endocrinology medicine.anatomical_structure Endometrial Hyperplasia Cancer research Female |
| Zdroj: | International Journal of Gynecological Pathology. 22:240-247 |
| ISSN: | 0277-1691 |
| DOI: | 10.1097/01.pgp.0000070851.25718.ec |
| Popis: | Cold-inducible RNA-binding protein (CIRP), an 18-kD protein in the mouse and human, is induced by lowering the temperature of cultured cells. CIRP is possibly a cell cycle regulator because its overexpression results in prolongation of G1 phase in vitro. We investigated the immunohistochemical expression of CIRP in 39 endometrial carcinomas, 12 endometrial hyperplasias, and 27 normal endometria using polyclonal antibody against CIRP and confirmed by Western blot analysis. CIRP was localized in the nuclei of glandular, stromal, and endothelial cells. The intensity of CIRP expression in glandular cells during the menstrual cycle was inversely proportional to its proliferative (Ki-67) activity, whereas it remained unchanged in stromal and vascular endothelial cells. The intensity of CIRP expression in hyperplastic glands was variable, whereas CIRP expression was absent or markedly reduced in most of the endometrial carcinomas. These results suggest that CIRP may participate in the cell cycle regulation of normal endometrium and the loss of its expression may be involved in endometrial carcinogenesis. |
| Databáze: | OpenAIRE |
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