CEA and NCA expressed by colon carcinoma cells affect their interaction with and lysability by activated lymphocytes

Int J Biol Markers. 1992 Jul-Sep;7(3):143-7. doi: 10.1177/172460089200700304.

Abstract

Heterogeneous lysability by interleukin-2 activated lymphocytes (LAK) and other immune effectors was observed in the human colon-carcinoma lines LoVo/Dx, LoVo/H and HT29. The tumor cells with high susceptibility to LAK (LoVo/Dx, HT29) expressed higher amounts of the adhesion molecules ICAMl, LFA3 and NCA/CEA than cells with low LAK sensitivity (LoVo/H). Monoclonal antibodies against these molecules caused a marked reduction of lysis by LAK of LoVo/Dx and HT29. A pool of these antibodies induced a nearly complete inhibition of the LAK lysis of both lines. Treatment of LoVo/Dx with differentiating agents (dimethylformamide and retinoic acid) led to a decreased expression of the adhesion molecules, including NCA, accompanied by increased resistance to LAK-mediated lysis. Moreover, the presence of CEA soluble antigen drastically inhibited the cytotoxic activity of LAK effectors against HT29 and LoVo/Dx cells, in a dose-dependent manner. These data indicate that sensitivity of colon-carcinoma cells to activated lymphocytes depends on the level of expression of adhesion molecules, including CEA and NCA. Given the role of CEA-related antigens in tumor/lymphocyte interaction, soluble CEA, frequently released by colon-carcinoma, may be involved in immunosuppressive effects induced in vivo by tumor cells.

MeSH terms

  • Antigens, Neoplasm / biosynthesis
  • Antigens, Neoplasm / drug effects
  • Antigens, Neoplasm / physiology*
  • Carcinoembryonic Antigen / biosynthesis
  • Carcinoembryonic Antigen / drug effects
  • Carcinoembryonic Antigen / physiology*
  • Cell Adhesion Molecules / biosynthesis
  • Cell Adhesion Molecules / drug effects
  • Cell Adhesion Molecules / physiology*
  • Colonic Neoplasms / immunology*
  • Colonic Neoplasms / metabolism
  • Cytotoxicity, Immunologic / physiology*
  • Dimethylformamide / pharmacology
  • Humans
  • Immune Tolerance / physiology
  • Killer Cells, Lymphokine-Activated / immunology*
  • Membrane Glycoproteins / biosynthesis
  • Membrane Glycoproteins / drug effects
  • Membrane Glycoproteins / physiology*
  • Tretinoin / pharmacology
  • Tumor Cells, Cultured

Substances

  • Antigens, Neoplasm
  • Carcinoembryonic Antigen
  • Cell Adhesion Molecules
  • Membrane Glycoproteins
  • Tretinoin
  • Dimethylformamide