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.Study design
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).Results
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.Conclusions
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.