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• W2003298766 abstract "Overexpression of GSTpi and underexpression of Topo II expression are associated with multidrug resistance (MDR) phenotype through nontransporter pathway. Tryptanthrin, a quinazoline derivative, was reported to sensitize resistant cells to doxorubicin by downregulation of MDR1 expression. This study aims to extendedly investigate the effect of tryptanthrin on the role of nontransporter-based genes in determining the MDR response in doxorubicin-resistant MCF-7 cells (MCF-7/adr). Results show that tryptanthrin downregulates GSTpi expression and reduces glutathione S-transferase (GST) activity, but has no effect on Topo II expression. Less production of GSTpi decomposes the protein-protein interactions of GSTpi and c-jun NH2-terminal kinase (JNK). The resulting free-form JNK undergoes phosphorylation upon elevated intracellular doxorubicin accumulation and subsequently activates JNK-mediated apoptosis. In conclusion, in addition to transporter pathway, tryptanthrin reverses MDR partly by modulating GSTpi-related pathway, a nontransporter pathway, in MCF-7/adr cells. It indicates that tryptanthrin may act as a potential chemoadjuvant agent through multiple targets." @default.
• W2003298766 created "2016-06-24" @default.
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• W2003298766 date "2009-06-01" @default.
• W2003298766 modified "2023-09-24" @default.
• W2003298766 title "Downregulation of GSTπ expression by tryptanthrin contributing to sensitization of doxorubicin-resistant MCF-7 cells through c-jun NH2-terminal kinase-mediated apoptosis" @default.
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• W2003298766 doi "https://doi.org/10.1097/cad.0b013e32832a2cd4" @default.
• W2003298766 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19318911" @default.
• W2003298766 hasPublicationYear "2009" @default.
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