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- W2009028105 abstract "Beta-Catenin is a critical transducer of the Wnt signal pathway and plays an important role in many developmental and cellular processes. Deregulation of beta-catenin signaling has been observed in a broad range of human tumors. In this report, we investigated whether tyrosine kinase inhibitor STI-571 could inhibit the beta-catenin signaling activity and hence suppress cell proliferation. Our results demonstrated that STI-571 effectively inhibited the constitutive activity of beta-catenin signaling in human colon cancer cells as well as the Wnt1-induced activation of beta-catenin signaling in HOS, HTB-94, and HEK 293 cells. Furthermore, STI-571 was shown to effectively suppress the proliferation of human colon cancer cells. Finally, we demonstrated that the Wnt1-mediated activation of a GAL4-beta-catenin heterologous transcription system was effectively inhibited by STI-571. Thus, our findings suggest that tyrosine phosphorylation may play an important role in regulating beta-catenin signaling activity, and inhibition of this signaling pathway by STI-571 may be further explored as an important target for alternative/adjuvant treatments for a broader range of human cancer." @default.
- W2009028105 created "2016-06-24" @default.
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- W2009028105 date "2003-04-01" @default.
- W2009028105 modified "2023-10-18" @default.
- W2009028105 title "Tyrosine kinase inhibitor STI-571/Gleevec down-regulates the β-catenin signaling activity" @default.
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- W2009028105 doi "https://doi.org/10.1016/s0304-3835(03)00013-2" @default.
- W2009028105 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4527752" @default.
- W2009028105 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12706873" @default.
- W2009028105 hasPublicationYear "2003" @default.
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