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Title of Journal: Mol Cell Biochem

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Abbravation: Molecular and Cellular Biochemistry

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Springer US

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DOI

10.1016/0378-5955(94)90285-2

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ISSN

1573-4919

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44Chloro2methylphenoxyEmphasis Type="Itali

Authors: Khadijeh BijangiVishehsaraei Mohammad Reza Saadatzadeh Su Huang Michael P Murphy Ahmad R Safa
Publish Date: 2010/05/06
Volume: 342, Issue: 1-2, Pages: 133-142
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Abstract

Cellular FLICE FADDlike IL1βconverting enzymeinhibitory protein cFLIP is a major resistance factor for the tumor necrosis factorrelated apoptosisinducing ligand TRAIL and in drug resistance in human malignancies cFLIP is an antagonist of caspases8 and 10 which inhibits apoptosis and is expressed as long cFLIPL and short cFLIPS splice forms cFLIP is often overexpressed in various human cancers including breast cancer Several studies have shown that silencing cFLIP by specific siRNAs sensitizes cancer cells to TRAIL and anticancer agents However systemic use of siRNA as a therapeutic agent is not practical at present In order to reduce or inhibit cFLIP expression small molecules are needed to allow targeting cFLIP without inhibiting caspases8 and 10 We used a small molecule inhibitor of cFLIP 44chloro2methylphenoxyNhydroxybutanamide CMH and show that CMH but not its inactive analog downregulated cFLIPL and cFLIPS mRNA and protein levels caused polyADPribose polymerase PARP degradation reduced cell survival and induced apoptosis in MCF7 breast cancer cells These results revealed that cFLIP is a critical apoptosis regulator that can serve as a target for small molecule inhibitors that downregulate its expression and serve as effective targeted therapeutics against breast cancer cells

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