ArticleJournal of cancer research and clinical oncology2008
Paclitaxel (Taxol)-induced apoptosis in human epithelioid sarcoma cell lines is enhanced by upregulation of CD95 ligand (FasL/Apo-1L).
Article in Journal of cancer research and clinical oncology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 10 citations in OpenAlex.
- The Fas-FasL system: from apoptosis regulator to therapeutic target in autoimmunity, cancer, and transplantation.Immunologic research · 2026Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeMetastasizing epithelioid sarcoma (ES) is an extremely aggressive tumor, because conventional chemotherapy and irradiation are largely ineffective. Here, we analyzed the impact of the CD95-mediated drug-induced apoptosis in ES cell lines.
methodsThe effects of paclitaxel (Taxol) and 5-FU were determined by MTT assay. The extent of apoptosis was analyzed by light microscopy and Annexin V staining (flow cytometry). The expression of death receptors and ligands was defined by RT-PCR, Western blotting and flow cytometry.
resultsAll cell lines expressed CD95, but not the CD95 ligand. The CD95 activation resulted in apoptosis and cell death in all cell lines. Both paclitaxel and 5-FU are able to trigger apoptosis, and furthermore, to upregulate CD95, whereas only paclitaxel increases CD95 ligand expression. Neutralizing antibodies directed against CD95 ligand effectively inhibited paclitaxel-induced cell death, thereby providing evidence for a direct involvement of the CD95 system in paclitaxel-induced apoptosis.
conclusionsConcomitant upregulation of CD95 receptor and ligand may significantly enhance the response of ES to anticancer drugs. As evident from the differential response of our clonal ES subpopulations to paclitaxel and 5-FU, effective activation of the CD95 system depends on intrinsic properties of both the chemotherapeutic agent and target cell population.
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