The involvement of the sLe-a selectin ligand in the extravasation of human colorectal carcinoma cells

Tal Ben-David, Orit Sagi-Assif, Tsipi Meshel, Veronica Lifshitz, Ilana Yron, Isaac P. Witz*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

22 Scopus citations

Abstract

The extravasation of tumor cells is a pivotal stage in the formation of hematogenous metastasis. An interaction of selectins expressed on endothelial cells and selectin ligands expressed by tumor cells has been implicated to play a role in extravasation. In the present study we used a human-mouse model to prove the hypothesis that the selectin ligand sialyl Lewis-a (sLe-a) is indeed involved in the in vivo extravasation of colorectal carcinoma (CRC) cells. The results indicated that highly metastatic CRC cells expressing high levels of sLe-a extravasate more efficiently than non-metastatic CRC cells expressing low levels of sLe-a. It was also demonstrated that down regulating the expression levels of sLe-a in CRC cells by genetic manipulations, significantly reduced CRC extravasation. Non-specific effects of these manipulations were ruled out. The results of this study indicate that the arrest and adhesion of CRC cells, and possibly of other types of cancer cells as well, to endothelium depend on the expression of the selectin ligand sLe-a by the tumor cells.

Original languageEnglish
Pages (from-to)218-224
Number of pages7
JournalImmunology Letters
Volume116
Issue number2
DOIs
StatePublished - 15 Mar 2008

Funding

FundersFunder number
Arnold and Ruth Feuerstein
Ela Kodesz Institute for Research on Cancer Development and Prevention
Fainbarg Family Fund
Jacqueline Seroussi Memorial Foundation for Cancer Research
James J. Leibman and Rita S. Leibman Endowment Fund for Cancer Research
Natan Blutinger
Israel Cancer Association
Tel Aviv University
Ministry of Health, State of Israel

    Keywords

    • Colorectal carcinoma
    • Experimental lung metastases
    • Extravasation
    • Fucosylated selectin ligands

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