Abstract | BACKGROUND: RESULTS:
FLLL32 was found to be a potent inhibitor of STAT3 phosphorylation, STAT3 DNA binding activity, and the expression of STAT3 downstream target genes in vitro, leading to the inhibition of cell proliferation as well as the induction of Caspase-3 and PARP cleavages in human multiple myeloma, glioblastoma, liver cancer, and colorectal cancer cell lines. However, FLLL32 exhibited little inhibition on some tyrosine kinases containing SH2 or both SH2 and SH3 domains, and other protein and lipid kinases using a kinase profile assay. FLLL32 was also more potent than four previously reported JAK2 and STAT3 inhibitors as well as curcumin to inhibit cell viability in these cancer cells. Furthermore, FLLL32 selectively inhibited the induction of STAT3 phosphorylation by Interleukin-6 but not STAT1 phosphorylation by IFN-γ. CONCLUSION:
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Authors | Li Lin, Stephanie Deangelis, Elizabeth Foust, James Fuchs, Chenglong Li, Pui-Kai Li, Eric B Schwartz, Gregory B Lesinski, Don Benson, Jiagao Lü, Dale Hoyt, Jiayuh Lin |
Journal | Molecular cancer
(Mol Cancer)
Vol. 9
Pg. 217
(Aug 16 2010)
ISSN: 1476-4598 [Electronic] England |
PMID | 20712901
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- FLLL 32
- STAT3 Transcription Factor
- STAT3 protein, human
- DNA
- Curcumin
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Topics |
- Cell Division
(drug effects)
- Cell Line, Tumor
- Curcumin
(analogs & derivatives, pharmacology)
- DNA
(drug effects, metabolism)
- Humans
- Phosphorylation
- STAT3 Transcription Factor
(antagonists & inhibitors, metabolism)
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