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.
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.
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.