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Expression of the CD44v2-10 Isoform Confers a Metastatic Phenotype

Importance of the Heparan Sulfate Attachment Site CD44v3¹

Cancer Metastasis Laboratory, University of Queensland and the Queensland Institute of Medical Research, Brisbane, Queensland, 4029 [A. P. B., J. A. R., T. M. A.]; Department of Surgery, Princess Alexandra Hospital, Woolloongabba, Queensland, 4102 [A. P. B., J. F., D. C. G.]; and Department of Pathology, University of Queensland, Brisbane, Queensland, 4029 [M. D. W.] Australia

We expressed the full-length CD44v2-10 isoform in SKHep1 cells, a nonmetastatic human hepatocellular carcinoma cell line that does not express any endogenous CD44v isoforms.In SCID mice, expression of CD44v2-10 by SKHep1 cells had no effect on s.c. primary tumor development but caused pulmonary metastases in 41% (7 of 17) of animals compared with control SKHep1 cells (0 of 16; P < 0.01). CD44v2-10 expression by SKHep1 cells resulted in enhanced heparan sulfate (HS) attachment and an enhanced capacity to bind heparin-binding growth factors. Mutation of the v3 domain to prevent HS attachment and growth factor binding abolished the metastatic phenotype, demonstrating that HS modification of CD44v2-10 plays a critical role in the development of metastases in this model. However, in vitro proliferation, motility, and invasion were not altered by CD44v2-10 expression.

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