Abstract
We examined the effects of troglitazone, one of thiazolidinedione derivatives on human basophilic leukemia cell line KU812. Troglitazone caused the suppression of cell growth, which was suggested to result from the decrease in cyclin E and the hyperphosphorylated form of retinoblastoma tumor suppressor gene product (pRb). In addition, troglitazone caused a decrease in histamine secretion due to the reduced expression of histidine decarboxylase mRNA. Peroxisome proliferator-activated receptor (PPAR)-gamma mRNA was undetectable by reverse transcription-polymerase chain reaction (RT-PCR) in KU812 cells. These findings suggested that troglitazone suppressed cell growth and histamine synthesis independently of PPARgamma.
MeSH terms
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Antineoplastic Agents / pharmacology*
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Cell Cycle / drug effects
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Cell Division / drug effects*
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Chromans / pharmacology*
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Cyclin E / drug effects
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Cyclin E / metabolism
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Dose-Response Relationship, Drug
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Gene Expression Regulation / drug effects
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Histamine / metabolism
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Humans
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RNA, Messenger / drug effects
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Receptors, Cytoplasmic and Nuclear / drug effects*
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Receptors, Cytoplasmic and Nuclear / genetics
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Receptors, Cytoplasmic and Nuclear / metabolism
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Thiazoles / pharmacology*
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Thiazolidinediones*
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Transcription Factors / drug effects*
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Transcription Factors / genetics
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Transcription Factors / metabolism
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Troglitazone
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Tumor Cells, Cultured
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U937 Cells
Substances
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Antineoplastic Agents
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Chromans
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Cyclin E
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RNA, Messenger
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Receptors, Cytoplasmic and Nuclear
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Thiazoles
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Thiazolidinediones
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Transcription Factors
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Histamine
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Troglitazone