Abstract
In the present study, we describe the cytotoxicity of the new drug prodigiosin (PG) in two small cell lung carcinoma (SCLC) cell lines, GLC4 and its derived doxorubicin-resistant GLC4/ADR cell line, which overexpresses multidrug-related protein 1 (MRP-1). We observed through Western blot that PG mediated cytochrome c release, caspase cascade activation and PARP cleavage, thereby leading to apoptosis in a dose-response manner. MRP-1 expression increased after PG treatment, although that does not lead to protein accumulation. The MTT assay showed no difference in sensitivity to PG between the two cell lines. Our results support PG as a potential drug for the treatment of lung cancer as it overcomes the multidrug resistance phenotype produced by MRP-1 overexpression.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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ATP Binding Cassette Transporter, Subfamily B, Member 1 / metabolism
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Anti-Bacterial Agents / therapeutic use*
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Antibiotics, Antineoplastic / therapeutic use*
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Apoptosis / drug effects*
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Carcinoma, Small Cell / drug therapy*
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Carcinoma, Small Cell / pathology
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Caspases / metabolism
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Cytochromes c / metabolism
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Doxorubicin / therapeutic use*
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Drug Resistance, Neoplasm*
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Enzyme Activation / drug effects
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Humans
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Lung Neoplasms / drug therapy*
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Lung Neoplasms / pathology
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Poly(ADP-ribose) Polymerases / metabolism
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Prodigiosin / therapeutic use*
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Tumor Cells, Cultured
Substances
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ATP Binding Cassette Transporter, Subfamily B, Member 1
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Anti-Bacterial Agents
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Antibiotics, Antineoplastic
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Doxorubicin
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Cytochromes c
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Poly(ADP-ribose) Polymerases
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Caspases
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Prodigiosin