Retinoic acid protects human breast cancer cells against etoposide-induced apoptosis by NF-kappaB-dependent but cIAP2-independent mechanisms.

Molecular Cancer
Ana M Jiménez-LaraHinrich Gronemeyer

Abstract

Retinoids, through their cognate nuclear receptors, exert potent effects on cell growth, differentiation and apoptosis, and have significant promise for cancer therapy and chemoprevention. These ligands can determine the ultimate fate of target cells by stimulating or repressing gene expression directly, or indirectly through crosstalking with other signal transducers. Using different breast cancer cell models, we show here that depending on the cellular context retinoids can signal either towards cell death or cell survival. Indeed, retinoids can induce the expression of pro-apoptotic (i.e. TRAIL, TNF-Related Apoptosis-Inducing Ligand, Apo2L/TNFSF10) and anti-apoptotic (i.e. cIAP2, inhibitor of apoptosis protein-2) genes. Promoter mapping, gel retardation and chromatin immunoprecipitation assays revealed that retinoids induce the expression of this gene mainly through crosstalk with NF-kappaB. Supporting this crosstalk, the activation of NF-kappaB by retinoids in T47D cells antagonizes the apoptosis triggered by the chemotherapeutic drugs etoposide, camptothecin or doxorubicin. Notably apoptosis induced by death ligands (i.e. TRAIL or antiFAS) is not antagonized by retinoids. That knockdown of cIAP2 expression by small interfe...Continue Reading

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Citations

Jun 8, 2012·Cancer Cell International·Ammad Ahmad FarooqiMuhammad Ismail
Oct 15, 2010·Expert Review of Anticancer Therapy·Oded Ben-AmotzSarah Kraus
Jan 29, 2016·Toxicology in Vitro : an International Journal Published in Association with BIBRA·Yanling ChenMenghang Xia
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Mar 13, 2014·Molecular Biology Reports·Abu Hena Mostafa KamalKwang-Hee Bae

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Methods Mentioned

BETA
FACS
flow cytometry
transfection
electrophoretic mobility shift
ChIPs
PCR
immunoprecipitation
acetylation
ChIP

Software Mentioned

Microsoft Excell

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