Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 176-182 |
| Number of pages | 7 |
| Journal | Gynecologic Oncology |
| Volume | 76 |
| Issue number | 2 |
| DOIs | |
| State | Published - Feb 2000 |
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Keywords
- Complement receptor type 1 (CR1, CD35)
- Decay-accelerating factor (DAF, CD55)
- Endometrial cancer
- Membrane cofactor protein (MCP, CD46)
- Protectin (CD59)
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Expression of complement regulatory proteins - CD 35, CD 46, CD 55, and CD 59 - In benign and malignant endometrial tissue. / Murray, Karuna P.; Mathure, Shephali; Kaul, Rashmi; Khan, Shah; Carson, Linda F.; Twiggs, Leo B.; Martens, Mark G.; Kaul, Anil.
In: Gynecologic Oncology, Vol. 76, No. 2, 02.2000, p. 176-182.Research output: Contribution to journal › Article
TY - JOUR
T1 - Expression of complement regulatory proteins - CD 35, CD 46, CD 55, and CD 59 - In benign and malignant endometrial tissue
AU - Murray, Karuna P.
AU - Mathure, Shephali
AU - Kaul, Rashmi
AU - Khan, Shah
AU - Carson, Linda F.
AU - Twiggs, Leo B.
AU - Martens, Mark G.
AU - Kaul, Anil
PY - 2000/2
Y1 - 2000/2
N2 - 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.
AB - 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.
KW - Complement receptor type 1 (CR1, CD35)
KW - Decay-accelerating factor (DAF, CD55)
KW - Endometrial cancer
KW - Membrane cofactor protein (MCP, CD46)
KW - Protectin (CD59)
UR - http://www.scopus.com/inward/record.url?scp=0033974021&partnerID=8YFLogxK
U2 - 10.1006/gyno.1999.5614
DO - 10.1006/gyno.1999.5614
M3 - Article
C2 - 10637067
AN - SCOPUS:0033974021
VL - 76
SP - 176
EP - 182
JO - Gynecologic Oncology
JF - Gynecologic Oncology
SN - 0090-8258
IS - 2
ER -