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[Cancer Research 61, 7356-7362, October 1, 2001]
© 2001 American Association for Cancer Research

Tumor Biology

Expression of the Antiangiogenic Factor 16K hPRL in Human HCT116 Colon Cancer Cells Inhibits Tumor Growth in Rag1-/- Mice1

Frauke Bentzien2, Ingrid Struman, Jean-François Martini, Joseph Martial and Richard Weiner

Center for Reproductive Sciences, University of California School of Medicine, San Francisco, California 94143 [F. B., J-F. M., R. W.], and Laboratoire de Biologie Moléculaire et de Génie Génétique, Université de Liège, B-4000 Sart Tilman, Belgium [I. S., J. M.]

The Mr 16,000 NH2-terminal fragment of human prolactin (16K hPRL) is a potent antiangiogenic factor inhibiting endothelial cell function in vitro and neovascularization in vivo. The present study was undertaken to test the ability of 16K hPRL to inhibit the growth of human HCT116 colon cancer cells transplanted s.c. into Rag1-/- mice. For this purpose, HCT116 cells were stably transfected with an expression vector encoding a peptide that included the signal peptide and first 139 amino acid residues of human prolactin (HCT11616K). Stable clones of HCT11616K cells secreted large amounts of biologically active 16K hPRL into the culture medium. Growth of HCT11616K cells in vitro was not different from wild-type HCT116 (HCT116wt) or vector-transfected HCT116 (HCT116vector) cells. Addition of recombinant 16K hPRL had no effect on the proliferation of HCT116wt cells in vitro. Tumor growth of HCT11616K cells implanted into Rag1-/- mice was inhibited 63% in four separate experiments compared with tumors formed from HCT116wt or HCT116vector cells. Inhibition of tumor growth of HCT11616K cells was correlated with a decrease in microvascular density by 44%. These data demonstrate that biologically active 16K hPRL can be expressed and secreted from human colon cancer cells using a gene transfer approach and that production of 16K hPRL by these cells was capable of inhibiting tumor growth and neovascularization. These findings support the potential of 16K hPRL as a therapeutic agent for the treatment of colorectal cancer.




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Copyright © 2001 by the American Association for Cancer Research.