Abstract
The effect of SN-38 was evaluated on multiple lung cancer cell lines. It inhibits anchorage-dependent and -independent growth as monitored by MTT and soft agar colony assay, respectively. SN-38 collapsed the mitochondrial membrane potential (MMP), arrested cells in S- and G2-phases of the cell cycle, and induced apoptosis via activation of caspase 3 and PARP. A single injection of 2 mg/kg body weight of SN-38 caused a significant reduction of lung cancer xenografts. These findings indicate that SN-38 induces apoptosis in the lung cancer cells effectively. Thus, SN-38 can potentially be an effective therapeutic agent against lung cancer.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antineoplastic Agents, Alkylating / pharmacology*
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Apoptosis / drug effects
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Camptothecin / analogs & derivatives*
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Camptothecin / pharmacology
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Carcinoma, Lewis Lung / drug therapy
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Carcinoma, Lewis Lung / pathology
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Carcinoma, Non-Small-Cell Lung / drug therapy*
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Carcinoma, Non-Small-Cell Lung / pathology
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Caspase 3 / physiology
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Cell Cycle / drug effects
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Cell Line, Tumor
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Cell Proliferation / drug effects
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Female
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Humans
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Irinotecan
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Lung Neoplasms / drug therapy*
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Lung Neoplasms / pathology
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Membrane Potential, Mitochondrial / drug effects
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Mice
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Mice, Inbred C57BL
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Poly(ADP-ribose) Polymerases / physiology
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Topoisomerase I Inhibitors / pharmacology*
Substances
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Antineoplastic Agents, Alkylating
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Topoisomerase I Inhibitors
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Irinotecan
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Poly(ADP-ribose) Polymerases
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Caspase 3
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Camptothecin