Expression of Complement Regulatory Proteins—CD 35, CD 46, CD 55, and CD 59—in Benign and Malignant Endometrial Tissue

• Published in: Gynecologic oncology Vol. 76; no. 2; pp. 176 - 182
• Main Authors: Murray, Karuna P., Mathure, Shephali, Kaul, Rashmi, Khan, Shah, Carson, Linda F., Twiggs, Leo B., Martens, Mark G., Kaul, Anil
• Format: Journal Article Conference Proceeding
• Language: English
• Published: San Diego, CA Elsevier Inc 01.02.2000; Elsevier
• Subjects: Adult; Aged; Aged, 80 and over; Antigens, CD - metabolism; Antigens, Neoplasm - metabolism; Biological and medical sciences; CD55 Antigens - metabolism; CD59 Antigens - metabolism; complement receptor type 1 (CR1, CD35); decay-accelerating factor (DAF, CD55); endometrial cancer; Endometrial Neoplasms - immunology; Endometrial Neoplasms - metabolism; Endometrium - immunology; Endometrium - metabolism; Female; Female genital diseases; Gynecology. Andrology. Obstetrics; Humans; Medical sciences; Membrane Cofactor Protein; membrane cofactor protein (MCP, CD46); Membrane Glycoproteins - metabolism; Middle Aged; Neoplasm Proteins - metabolism; protectin (CD59); Receptors, Complement 3b - metabolism; Tumors; endometrial cancer; decay-accelerating factor (DAF, CD55); complement receptor type 1 (CR1, CD35); protectin (CD59); membrane cofactor protein (MCP, CD46); Human; Immunohistochemistry; Carcinoma; Complement; Malignant tumor; Regulator; Carcinogenesis; Protein; Female genital diseases; Decay accelerating factor; Pathology; Image analysis; Uterine diseases; Membrane cofactor protein; Female; Endometrium; Comparative study; Biological receptor
• ISSN: 0090-8258; 1095-6859
• DOI: 10.1006/gyno.1999.5614

Objective.Complement system plays an important role in host defense mechanisms against microorganisms and tumor cells. To protect themselves from autologous complement-mediated damage, normal host tissues express cell membrane-associated complement regulatory proteins (CRPs). To investigate whether neoplastic endometrial tissues overexpress these proteins to escape complement damage, we examined the distribution of complement receptor type 1 (CR1, CD35), membrane cofactor protein (MCP, CD46), decay-accelerating factor (DAF, CD55), and protectin (MACIF, CD59) on frozen endometrial tissue samples. Methods. A total of 54 endometrial tissue samples were collected. Cryosections were obtained of 31 benign and 23 malignant tissue specimens. Tissue sections were stained by immunohistochemical staining procedure using specific antibodies and employing the avidin–biotin technique. Quantitation of the protein content of these CRPs was determined using the Samba 4000 image analysis system. Results. For all four of the CRPs studied, a statistically significant difference in protein expression between the benign and malignant endometrial tissue 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 tissues. The upregulation of these CRPs may promote resistance of the endometrial malignant tissue to complement-mediated damage, thereby allowing the tumor cells to escape from cytolysis and thus promoting carcinogenesis.