Role of calcium in E-selectin induced phenotype of T84 colon carcinoma cells

Biochem Biophys Res Commun. 2003 Feb 21;301(4):907-14. doi: 10.1016/s0006-291x(03)00062-7.


The adhesion of cancer cells to the endothelium during the metastatic process involves the interaction of specific cell-cell adhesion receptors on the cell surface. E-selectin on endothelial cells and sialyl Lewis X carbohydrate component on tumor cells are mainly implicated in the adhesion of colon carcinoma cells to the endothelium of target organ. In this paper we show that binding of E-selectin to T84 colon tumor cells causes approximately a twofold increase in intracellular calcium concentration. In particular, using two inhibitors of receptor operated calcium channels, CAI and SK&F 96365, we present evidences that the augmentation in cytoplasmic calcium originates from ionic influx from extracellular sources. Furthermore, we demonstrated that modulation of [Ca2+]i by engagement of E-selectin receptor starts signal transduction pathways that affect cell spreading, tyrosine phosphorylation signaling, and cancer cell motility.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Calcium / metabolism*
  • Calcium Channel Blockers / pharmacology
  • Calcium Signaling / drug effects
  • Cell Movement / drug effects
  • Colonic Neoplasms / drug therapy
  • Colonic Neoplasms / metabolism*
  • Colonic Neoplasms / pathology
  • E-Selectin / pharmacology*
  • Humans
  • Imidazoles / pharmacology
  • Phenotype
  • Phosphorylation
  • Recombinant Proteins / pharmacology
  • Triazoles / pharmacology
  • Tumor Cells, Cultured
  • Tyrosine / metabolism


  • Antineoplastic Agents
  • Calcium Channel Blockers
  • E-Selectin
  • Imidazoles
  • Recombinant Proteins
  • Triazoles
  • Tyrosine
  • carboxyamido-triazole
  • 1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole
  • Calcium