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Semaphorin 3F Gene from Human 3p21.3 Suppresses Tumor Formation in Nude Mice¹

Department of Cellular and Structural Biology, The University of Texas Health Science Center, San Antonio, Texas 78229-3900 [R. X., A. R. D., C. H. H., S. L. N.]; Lawrence Berkeley National Laboratory, Berkeley, California 94720 [A. R. D.]; Myriad Genetics, Salt Lake City, Utah 84108 [C. H. H.]; Department of Pathology, Jinling Hospital, Nanjing University School of Medicine, Nanjing 210002, P.R. China [X-J. Z.]; and Sagres Discovery Davis, California 95616 [C. T.]

Loss of heterozygosity on human chromosome 3p21.3 is a frequent occurrence in manytumor types. In a previous study, our laboratory demonstrated that an 80-kb P1 clone from chromosome 3 suppresses the tumorigenicity of the mouse fibrosarcoma cell line A9. Two cDNAs corresponding to genes encoded on this P1 clone, semaphorin 3F (SEMA3F) and N23, were tested for their effects on in vitro and in vivo growth characteristics after transfection into mouse A9 cells. Transfection of SEMA3F cDNA resulted in complete loss of tumorigenicity in nude mice, whereas transfection of N23 had no effect. Moreover, SEMA3F also functioned to block apoptosis of transfected A9 cells treated with Taxol or Adriamycin. The human ovarian adenocarcinoma cell line HEY showed a similar result as A9 cells, but the small cell lung cancer line GLC45 was unaffected by expression of SEMA3F.

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