The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1998/9/1185/ $5.00
The Journal of Experimental Medicine, Volume 188, Number 6, September 21, 1998 1185-1190


Brief Definitive Reports

APRIL, a New Ligand of the Tumor Necrosis Factor Family, Stimulates Tumor Cell Growth

Michael Hahne*, Takao Kataoka*, Michael Schröter*, Kay Hofmann§, Martin Irmler*, Jean-Luc Bodmer*, Pascal Schneider*, Tierry Bornand*, Nils Holler*, Lars E. French||, Bernard Sordat§, Donata Rimoldi{ddagger}, and Jürg Tschopp*

From the * Institute of Biochemistry, the {ddagger} Ludwig Institute of Cancer Research, Lausanne Branch, University of Lausanne, CH-1066 Epalinges, Switzerland; the § Swiss Institute for Experimental Cancer Research, BIL Research Centre, CH-1066 Epalinges, Switzerland; and the || Department of Dermatology, University of Geneva, Medical School, CH-1211 Geneva 4, Switzerland

Members of the tumor necrosis factor (TNF) family induce pleiotropic biological responses, including cell growth, differentiation, and even death. Here we describe a novel member of the TNF family designated APRIL (for a proliferation-inducing ligand). Although transcripts of APRIL are of low abundance in normal tissues, high levels of mRNA are detected in transformed cell lines, and in human cancers of colon, thyroid, and lymphoid tissues in vivo. The addition of recombinant APRIL to various tumor cells stimulates their proliferation. Moreover, APRIL-transfected NIH-3T3 cells show an increased rate of tumor growth in nude mice compared with the parental cell line. These findings suggest that APRIL may be implicated in the regulation of tumor cell growth.

Key Words: tumor necrosis factor • tumorigenesis • cell survival • ligand • protein


Address correspondence to Dr. Jürg Tschopp, Institute of Biochemistry, University of Lausanne, Ch. des Boveresses 155, CH-1066 Epalinges, Switzerland. Phone: 41-21-692-5738; Fax: 41-21-692-5705; E-mail: jurg.tschopp{at}ib.unil.ch

T. Kataoka, M. Schröter, K. Hofmann, and M. Irmler contributed equally to this work.


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