AI Article Synopsis
- The study examines the effects of prodigiosin (PG) on two small cell lung carcinoma (SCLC) cell lines, including a doxorubicin-resistant variant that overexpresses MRP-1.
- PG triggers apoptosis by activating a series of biological processes, including cytochrome c release and caspase activation, in both cell lines tested.
- The findings suggest that PG may be effective for treating lung cancer as it effectively counters the challenges posed by MRP-1 related multidrug resistance.
Article 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.
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| http://dx.doi.org/10.1097/00001813-200504000-00005 | DOI Listing |
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