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Blood, 1 December 2006, Vol. 108, No. 12, pp. 3700-3706.
Prepublished online as a Blood First Edition Paper on August 24, 2006; DOI 10.1182/blood-2006-03-011973.
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Submitted March 23, 2006
Accepted July 24, 2006
Wogonin sensitizes resistant malignant cells to
TNF - and TRAIL-induced apoptosis
Stefanie C Fas, Sven Baumann, Jia Yun Zhu, Marco Giaisi, Monika K Treiber, Ulrich Mahlknecht, Peter H Krammer, and Min Li-Weber*
Tumorimmunology Program, German Cancer Research Center, Heidelberg, Germany
German Cancer Research Center D030
Department of Hematology/Oncology, University of Heidelberg Medical Center, Heidelberg, Germany
* Corresponding author; email: m.li-weber{at}dkfz-heidelberg.de.
TNF has previously been used in anti-cancer therapy. However, the therapeutic application of TNF was largely limited due to its general toxicity and the fact that it activates the NF- B-family transcription factors which are pro-inflammatory and anti-apoptotic. To overcome this problem in vitro, specific NF-B inhibitors, transcription or protein synthesis inhibitors such as actinomycin D and cycloheximide are usually used in combination to increase TNF-killing of tumor cells. However, these agents also cause harmful side effects in vivo. We show here that wogonin, derived from the popular Chinese herb Huang-Qin, attenuates NF-B activity by shifting TNF-induced free radical O2 to a more reduced non-radical product H2O2 and thereby sensitizes TNF-resistant leukemia cells to TNF-induced apoptosis. Importantly, wogonin does not affect the viability of normal peripheral blood T cells. Wogonin also sensitizes TRAIL-induced apoptosis. Our data suggest a potential use of wogonin as a TNF or TRAIL adjuvant for cancer treatment. Our data also demonstrate how an herbal compound enhances killing of tumor cells at reduced side effects compared to other treatments.
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