@article{Frese2002Enhan-14293,
  year={2002},
  doi={10.1067/mtc.2002.119694},
  title={Enhancement of Apo2L/TRAIL (tumor necrosis factor–related apoptosis-inducing ligand)–induced apoptosis in non–small cell lung cancer cell lines by chemotherapeutic agents without correlation to the expression level of cellular protease caspase-8 inhibitory protein},
  number={1},
  volume={123},
  issn={0022-5223},
  journal={The Journal of Thoracic and Cardiovascular Surgery},
  pages={168--174},
  author={Frese, Steffen and Brunner, Thomas and Gugger, Mathias and Uduehi, Aima and Schmid, Ralph A.}
}

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    <dc:contributor>Uduehi, Aima</dc:contributor>
    <dc:contributor>Frese, Steffen</dc:contributor>
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    <dcterms:title>Enhancement of Apo2L/TRAIL (tumor necrosis factor–related apoptosis-inducing ligand)–induced apoptosis in non–small cell lung cancer cell lines by chemotherapeutic agents without correlation to the expression level of cellular protease caspase-8 inhibitory protein</dcterms:title>
    <dc:creator>Schmid, Ralph A.</dc:creator>
    <dc:contributor>Schmid, Ralph A.</dc:contributor>
    <dc:contributor>Gugger, Mathias</dc:contributor>
    <dc:creator>Brunner, Thomas</dc:creator>
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    <dc:creator>Gugger, Mathias</dc:creator>
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    <dcterms:abstract xml:lang="eng">Objective:&lt;br /&gt;Apo2L/tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) is a potential anticancer drug that promotes apoptosis specifically in tumor cells. Because not all cancer cells are susceptible to Apo2L/TRAIL, the aim of our study was to determine whether non–small cell lung cancer cells can be sensitized by chemotherapeutic agents for Apo2L/TRAIL-induced apoptosis. In addition, endogenous expression levels of the caspase-inhibiting cellular protease caspase-8 inhibitory protein (C-FLIP) were measured to investigate partial resistance to Apo2L/TRAIL.&lt;br /&gt;Methods:&lt;br /&gt;Six human lung cancer cell lines (A549, NCI-H358, Calu1, Calu6, SkMes1, and SkLu1) were incubated with soluble Apo2L/TRAIL and two different concentrations each of cisplatin, paclitaxel, doxorubicin, 5-fluorouracil, and camptothecin. After 24 hours the rate of apoptosis was measured by annexin V/propidium iodide staining followed by FACScan analysis. Expression levels of C-FLIP in cell lines and lung cancer biopsy specimens were determined by Western blotting.&lt;br /&gt;Results:&lt;br /&gt;Treatment of lung cancer cells with Apo2L/TRAIL alone resulted in apoptotic cell death in four cell lines (P &lt; .001). Combining Apo2L/TRAIL and chemotherapeutic agents enhanced the rate of apoptosis significantly. Statistical analysis revealed a synergistic effect of Apo2L/TRAIL in combination with 1.8 mmol/L camptothecin and 100 μmol/L cisplatin, each in four of the six cell lines (P &lt; .002). Western blot analysis showed that sensitization to Apo2L/TRAIL did not correlate with the expression of cellular protease caspase-8 inhibitory protein. Furthermore, no increased cellular protease caspase-8 inhibitory protein levels relative to those in normal lung tissue could be found in non–small cell lung cancer specimens from 12 patients. Conclusion: Apo2L/TRAIL-induced apoptosis in non–small cell lung cancer cell lines is significantly enhanced by chemotherapeutic agents. Resistance and sensitization to Apo2L/TRAIL are not correlated with the endogenous expression level of cellular protease caspase-8 inhibitory protein, implying that in non–small cell lung cancer other mechanisms are responsible for inhibition of the Apo2L/TRAIL pathway. Even though the molecular mechanism remains unclear, the combination of Apo2L/TRAIL with chemotherapy may be a promising treatment modality for non–small cell lung cancer.</dcterms:abstract>
    <dcterms:bibliographicCitation>First publ. in: Journal of Thoracic and Cardiovascular Surgery ; 123 (2002), 1. - S. 168-174</dcterms:bibliographicCitation>
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    <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2011-10-21T11:56:22Z</dc:date>
    <dc:creator>Uduehi, Aima</dc:creator>
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    <dc:creator>Frese, Steffen</dc:creator>
    <dc:contributor>Brunner, Thomas</dc:contributor>
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