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Does Integrin-Mediated Cell Death Confer Tissue Tropism in Metastasis?

¹ Department of Genetics and Tumor Cell Biology, St. Jude Children's Research Hospital, Memphis, Tennessee and ² Department of Pathology, University of California at San Diego School of Medicine and The John and Rebecca Moores University of California at San Diego Cancer Center, La Jolla, California

Requests for reprints: Dwayne G. Stupack, Department of Pathology, University of California at San Diego School of Medicine and The John and Rebecca Moores University of California at San Diego Cancer Center, 3855 Health Science Drive MC0803, La Jolla, CA 92093-0803. Phone: 858-822-1150; Fax: 858-822-2630; E-mail: dstupack{at}ucsd.edu or Jill M. Lahti, Department of Genetics and Tumor Cell Biology, St. Jude Children's Hospital, 332 North Lauderdale MS350, Memphis, TN 38105. Phone: 901-495-3501; Fax: 901-495-2381; E-mail: jill.lahti{at}st.jude.org.

To develop metastatic capability, tumor cells must evolve the capacity to survive in novel microenvironments. Recently, we showed that metastasis of neuroblastoma cells is enhanced by loss of caspase-8, an event that occurs frequently in this malignancy. In poorly metastatic cells, unligated integrins were found to trigger activation of caspase-8, providing a selective pressure to promote its attenuation and thereby increased survival in foreign adhesive environments. Our findings suggest one mechanism by which the organotropism of metastastic cancer cells can arise. (Cancer Res 2006; 66(12): 5981-4)