Expression of complement regulatory proteins - CD 35, CD 46, CD 55, and CD59 - in benign and malignant endometrial tissue

Citation
Kp. Murray et al., Expression of complement regulatory proteins - CD 35, CD 46, CD 55, and CD59 - in benign and malignant endometrial tissue, GYNECOL ONC, 76(2), 2000, pp. 176-182
Citations number
26
Categorie Soggetti
Reproductive Medicine
Journal title
GYNECOLOGIC ONCOLOGY
ISSN journal
00908258 → ACNP
Volume
76
Issue
2
Year of publication
2000
Pages
176 - 182
Database
ISI
SICI code
0090-8258(200002)76:2<176:EOCRP->2.0.ZU;2-0
Abstract
Objective. Complement system plays an important role in host defense mechan isms against microorganisms and tumor cells. To protect themselves from aut ologous complement-mediated damage, normal host tissues express cell membra ne-associated complement regulatory proteins (CRPs). To investigate whether neoplastic endometrial tissues overexpress these proteins to escape comple ment damage, we examined the distribution of complement receptor type 1 (CR 1, CD35), membrane cofactor protein (MCP, CD46), decay-accelerating factor (DAF, CD55), and protectin (MACIF, CD59) on frozen endometrial tissue sampl es. Methods. A total of 54 endometrial tissue samples were collected. Cryosecti ons were obtained of 31 benign and 23 malignant tissue specimens. Tissue se ctions were stained by immunohistochemical staining procedure using specifi c antibodies and employing the avidin-biotin technique. Quantitation of the protein content of these CRPs was determined using the Samba 4000 image an alysis system. Results. For all four of the CRPs studied, a statistically significant diff erence in protein expression between the benign and malignant endometrial t issue specimens (P < 0.0001) was observed. Conclusions. Overexpression of all the CRPs studied (CD35, CD46, CD55, CD59 ) was observed in the malignant as compared with the benign endometrial tis sues. The upregulation of these CRPs may promote resistance of the endometr ial malignant tissue to complement-mediated damage, thereby allowing the tu mor cells to escape from cytolysis and thus promoting carcinogenesis. (C) 2 000 Academic Press.