Different phenotypes of colon carcinoma cells interacting with endothelial cells: role of E-selectin and ultrastructural data

Abstract

Adhesion molecules are intimately involved in the process of tumour progression. Among them, Eselectin is an inducible endothelial cell adhesion molecule that plays a role in the interactions of neoplastic cells with the endothelium. These interactions are required for the trans-endothelial migration of tumour cells that leads to the growth at the new sites. Since the detailed events in the early phase of metastasis still remain poorly defined, our study has undertaken an electron-microscopic analysis of the interactions of human colon carcinoma cells with endothelial cells as well as an analysis of the effect of recombinant purified E-selectin in the cell signalling involved in colon cancer cell malignant phenotype. Results revealed that SW480 and T84 colon cancer cell lines show different features, different adhesion kinetics, a different cytoskeletal organization, and a different tyrosine phosphorylation pattern when seeded on an endothelial cell monolayer or recombinant E-selectin. In particular T84 cancer cells adhere more efficiently to the E-selectin and this interaction is associated with pronounced morphological changes, actin redistribution and filopodial processes, and an increase in tyrosine phosphorylation of different proteins. These data support the hypothesis that E-selectin ligand is not only a cell-cell adhesion molecule but also initiates a signalling transduction pathway inside the cells.

Epithelial and mesenchymal phenotypic switchings modulate cell motility in metastasis

“…Attachment of cancer cells to the endothelium and subsequent formation of metastases can be inhibited by addition of antibodies against E-selectin (171). Furthermore, selectin-dependent adhesion to endothelial cells results in morphology changes, reorganization of the cytoskeleton, and tyrosine phosphorylation, suggesting that these interactions are not limited to adhesion and may have downstream signaling effects (172). Differential expression of selectin ligands can also influence the site of metastastic colonization and account for organotropism (173).…”

Intestinal Models for Personalized Medicine: from Conventional Models to Microfluidic Primary Intestine-on-a-chip

“…Ultrastructural examination showed that these cells have a rich microvillar surface, a moderate amount of intermediate filaments, a few desmosomes, few primary and many secondary lysosomes, and a well-developed intercellular lumina [ 47 ]. T84 colon carcinoma cells present considerable heterogeneity in their morphology, an irregular cellular surface, many large vesicles in the peripheral cytoplasm, pleomorphic microvilli, and well-demarcated enlarged nuclei [ 48 ]. Usually, results obtained from adenocarcinoma-derived immortalized cell lines cannot be directly applied to make conclusions about the responses of the living human intestine.…”

Minimal residual disease in prostate cancer patients after primary treatment: theoretical considerations, evidence and possible use in clinical management

“…The initial attachment is via selectins, the presentation of selectin ligands is thought to be crucial to extravasation, especially E-selectin [81]. This results in morphological changes in the tumor cells, reorganization of the cytoskeleton and tyrosine phosphorylation [82]. This suggests that downstream signaling effects occur as a result of cellular adhesion.…”