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Molecular and Cellular Biology, October 2000, p. 7826-7837, Vol. 20, No. 20
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

A Novel AP-1 Element in the CD95 Ligand Promoter Is Required for Induction of Apoptosis in Hepatocellular Carcinoma Cells upon Treatment with Anticancer Drugs

Sören T. Eichhorst,1 Martina Müller,2 Min Li-Weber,1 Henning Schulze-Bergkamen,2 Peter Angel,3 and Peter H. Krammer1,*

Tumor Immunology Program1 and Division of Signal Transduction German Cancer Research Center (DKFZ),3 69120 Heidelberg, and Department of Internal Medicine IV Hepatology and Gastroenterology, University Hospital, 69115 Heidelberg,2 Germany

Received 23 February 2000/Returned for modification 13 April 2000/Accepted 28 July 2000

The CD95 (also called APO-1 or Fas) system plays a major role in the induction of apoptosis in lymphoid and nonlymphoid tissues in response to a variety of extracellular signals, including chemotherapeutic drugs. Here we report that the CD95 ligand (CD95L) is upregulated in hepatoma cells upon treatment with antineoplastic drugs. Upregulation by different chemotherapeutic drugs is functionally relevant for drug-induced apoptosis and is mediated by transcriptional mechanisms. The MEKK1/JNKK pathway and a novel AP-1 element in the CD95L promoter downstream of the TATA box are required for CD95L upregulation. Thus, understanding the mechanisms of CD95-mediated apoptosis through CD95L upregulation upon treatment of hepatocellular carcinomas with chemotherapeutic drugs may contribute to the improvement of anticancer chemotherapy.

* Corresponding author. Mailing address: Division of Immunogenetics (G0300), German Cancer Research Center, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany. Phone: 49-6221-423718. Fax: 49-6221-411715. E-mail: P.Krammer{at}dkfz.de.

Molecular and Cellular Biology, October 2000, p. 7826-7837, Vol. 20, No. 20
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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