Ravindranath Naren M H, Shuler Charles
Center for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA 90033, USA.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2007 Feb;103(2):231-9. doi: 10.1016/j.tripleo.2006.05.028. Epub 2006 Oct 16.
Complement restriction factors (CD46, membrane cofactor; CD55, decay accelerating factor; and CD59, protectin) are overexpressed on tumor cells, and they enable tumor cells to escape from complement-dependent and antibody-mediated killing. Cell-surface density of complement restriction factors (CRFs) on oral squamous cell carcinoma (OSCC) is compared with that found on other solid tumors (breast, pancreas, colon carcinomas, and melanoma) to understand the significance of their diversity.
The cell-surface expression of CRFs on tumor cells was confirmed with confocal laser scan fluorescent microscopy. Cell suspension enzyme-linked immunosorbent assay (cs-ELISA), which measures the density of cell-surface antigens, was utilized to study CRFs on the cell surface of tumor cells (OSCC, 2 cell lines; breast, 5 cell lines; pancreas, 3 cell lines; colon, 3 cell lines; and melanoma, 9 cell lines).
Confocal laser scan fluorescent microscopy confirmed the expression of CD46, CD55, and CD59 on the cell surface of OSCC cell lines SCC12 and SCC71. The relative densities of cell-surface expression obtained from cs-ELISAs of CRFs on OSCCs are as follows: CD59 > CD55 > CD46. The relative densities of the 3 CRFs in breast and pancreatic carcinomas were similar to those found in OSCCs, whereas the profile of CRFs in melanoma (CD59 > CD55 < CD46) and colon cancer (CD46 > CD55 > CD59) were different.
These findings indicate diverse strategies adopted by tumor types to resist antibody-mediated complement-dependent cytotoxicity; possibly the factors (exogenous and endogenous) in their respective microenvironments may play a role in the diversity.
补体限制因子（CD46，膜辅因子；CD55，衰变加速因子；以及CD59，保护素）在肿瘤细胞上过度表达，使肿瘤细胞能够逃避补体依赖性和抗体介导的杀伤作用。比较口腔鳞状细胞癌（OSCC）上补体限制因子（CRFs）的细胞表面密度与其他实体瘤（乳腺癌、胰腺癌、结肠癌和黑色素瘤）上的情况，以了解其差异的意义。
通过共聚焦激光扫描荧光显微镜确认肿瘤细胞上CRFs的细胞表面表达。采用细胞悬浮酶联免疫吸附测定（cs-ELISA）来测量细胞表面抗原密度，以研究肿瘤细胞（OSCC，2种细胞系；乳腺癌，5种细胞系；胰腺癌，3种细胞系；结肠癌，3种细胞系；黑色素瘤，9种细胞系）表面的CRFs。
共聚焦激光扫描荧光显微镜证实了CD46、CD55和CD59在OSCC细胞系SCC12和SCC71细胞表面的表达。从OSCC的CRFs的cs-ELISA获得的细胞表面表达相对密度如下：CD59 > CD55 > CD46。乳腺癌和胰腺癌中3种CRFs的相对密度与OSCC中的相似，而黑色素瘤（CD59 > CD55 < CD46）和结肠癌（CD46 > CD55 > CD59）中CRFs的情况则不同。
这些发现表明不同肿瘤类型采用了多种策略来抵抗抗体介导的补体依赖性细胞毒性；可能其各自微环境中的因素（外源性和内源性）在这种差异中发挥了作用。
