In order to test this postulate, the expression of three important CAMs involved in tumor processes (CD44, ICAM-1 and LFA-3) in the human cancer cell lines HT29 (colon adenocarcinoma), A431 (squamous epidermal carcinoma) and A2780 (ovarian carcinoma) grown in monolayer or as multicellular spheroids was compared.
Within this population, we found that CD58 and CD44 were upregulated using a cDNA GeneChip, and CD44(high)CD58(high) cancer cells, the common existence of which was demonstrated by flow cytometry in multiple colon cancer cell lines and primary specimens, exhibited enhanced self-renewal ability, epithelial-mesenchymal transition ability and tumorigenicity, both in vitro and in vivo.
However, work on the Epstein-Barr virus (EBV)-associated malignancy Burkitt's lymphoma (BL) has suggested that down-regulation of one particular adhesion molecule, the lymphocyte function-associated antigen LFA-3, on the tumor cell surface is a key factor in allowing these target cells to escape EBV-specific T cell surveillance.