Colon‐cancer cell variants producing regressive tumors in syngeneic rats, unlike variants yielding progressive tumors, attach to interstitial collagens through integrin α 2 β 1

Nine clones of tumor cells, derived from a single rat colon carcinoma, were analyzed for their adhesive properties and in vivo growth patterns. Four clones (denoted REG) gave rise to regressively growing tumors. Cells from the 4 REG clones attached significantly better to collagen types I and III than did cells from the 5 clones (denoted PRO) which grew progressively in vivo . In contrast, REG and PRO clones did not differ in their attachment to collagen type IV, laminin or fibronectin. The attachment of REG cells to collagen was dependent on Mg 2+ , but not Ca 2+ . Monospecific rabbit IgG to rat integrin β 1 ‐chain inhibited REG cell attachment to collagen, demonstrating involvement of a β 1 integrin in this process. PRO and REG cells expressed an underglycosylated β 1 chain (M r ∼ 105,000) that was somewhat smaller than β 1 ‐chains described previously on rat fibroblasts and hepatocytes (M r ∼ 115,000). Monoclonal IgG to rat integrin α 2 β 1 , but not to α 1 β 1 , readily inhibited REG cell attachment to collagen, demonstrating the involvement of integrin α 2 β 1 . However, β 1 and α 2 integrin subunits were found in purified glycoproteins from both PRO and REG cells. This suggests that α 2 β 1 integrin is expressed by both cell variants, but is functional as a collagen receptor on REG cells only. In this system of tumor‐cell variants, the clear‐cut differences in attachment to interstitial collagens of the 9 clones suggest a possible relationship between this attachment and the capacity to induce progressive or regressive tumors. © 1996 Wiley‐Liss, Inc.