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See detailCurcumin-the paradigm of a multi-target natural compound with applications in cancer prevention and treatment
Teiten, Marie-Helene; Eifes, Serge UL; Dicato, Mario et al

in Toxins (2010), 79(4), 128-62

As cancer is a multifactor disease, it may require treatment with compounds able to target multiple intracellular components. We summarize here how curcumin is able to modulate many components of ... [more ▼]

As cancer is a multifactor disease, it may require treatment with compounds able to target multiple intracellular components. We summarize here how curcumin is able to modulate many components of intracellular signaling pathways implicated in inflammation, cell proliferation and invasion and to induce genetic modulations eventually leading to tumor cell death. Clinical applications of this natural compound were initially limited by its low solubility and bioavailability in both plasma and tissues but combination with adjuvant and delivery vehicles was reported to largely improve bio-availability of curcumin. Moreover, curcumin was reported to act in synergism with several natural compounds or synthetic agents commonly used in chemotherapy. Based on this, curcumin could thus be considered as a good candidate for cancer prevention and treatment when used alone or in combination with other conventional treatments. [less ▲]

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See detailChemopreventive potential of curcumin in prostate cancer
Teiten, Marie-Helene; Gaascht, Francois; Eifes, Serge UL et al

in Genes and Nutrition (2010), 5(1), 61-74

The long latency and high incidence of prostate carcinogenesis provides the opportunity to intervene with chemoprevention in order to prevent or eradicate prostate malignancies. We present here an ... [more ▼]

The long latency and high incidence of prostate carcinogenesis provides the opportunity to intervene with chemoprevention in order to prevent or eradicate prostate malignancies. We present here an overview of the chemopreventive potential of curcumin (diferuloylmethane), a well-known natural compound that exhibits therapeutic promise for prostate cancer. In fact, it interferes with prostate cancer proliferation and metastasis development through the down-regulation of androgen receptor and epidermal growth factor receptor, but also through the induction of cell cycle arrest. It regulates the inflammatory response through the inhibition of pro-inflammatory mediators and the NF-kappaB signaling pathway. These results are consistent with this compound's ability to up-induce pro-apoptotic proteins and to down-regulate the anti-apoptotic counterparts. Alone or in combination with TRAIL-mediated immunotherapy or radiotherapy, curcumin is also reported to be a good inducer of prostate cancer cell death by apoptosis. Curcumin appears thus as a non-toxic alternative for prostate cancer prevention, treatment or co-treatment. [less ▲]

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See detailGene expression profiling related to anti-inflammatory properties of curcumin in K562 leukemia cells
Teiten, Marie-Helene; Eifes, Serge UL; Reuter, Simone et al

in Annals of the New York Academy of Sciences (2009), 1171

A strong relationship exists between inflammation and carcinogenesis. To bring insights into the anti-inflammatory mechanisms by which chemopreventive agents, such as curcumin, are able to counteract the ... [more ▼]

A strong relationship exists between inflammation and carcinogenesis. To bring insights into the anti-inflammatory mechanisms by which chemopreventive agents, such as curcumin, are able to counteract the action of inflammation mediators, such as tumor necrosis factor-alpha (TNF-alpha), we compared gene expression profiles in K562 cells treated with curcumin-TNF-alpha versus TNF-alpha alone. Microarray data analysis revealed that, among the 376 differentially expressed genes by curcumin treatment, genes belonging to the cell cycle and the Janus kinase-signal transducer and activator of transcription signaling pathways were downregulated. This study also indicated that the upregulation of the heat shock family genes is highly implicated in the anti-inflammatory effect of curcumin. [less ▲]

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See detailTumor necrosis factor alpha induces gamma-glutamyltransferase expression via nuclear factor-kappaB in cooperation with Sp1
Reuter, Simone; Schnekenburger, Michael; Cristofanon, Silvia et al

in Biochemical Pharmacology (2009), 77(3), 397-411

Gamma-glutamyltransferase (GGT) cleaves the gamma-glutamyl moiety of glutathione (GSH), an endogenous antioxidant, and is involved in mercapturic acid metabolism and in cancer drug resistance when ... [more ▼]

Gamma-glutamyltransferase (GGT) cleaves the gamma-glutamyl moiety of glutathione (GSH), an endogenous antioxidant, and is involved in mercapturic acid metabolism and in cancer drug resistance when overexpressed. Moreover, GGT converts leukotriene (LT) C4 into LTD4 implicated in various inflammatory pathologies. So far the effect of inflammatory stimuli on regulation of GGT expression and activity remained to be addressed. We found that the proinflammatory cytokine tumor necrosis factor alpha (TNFalpha) induced GGT promoter transactivation, mRNA and protein synthesis, as well as enzymatic activity. Remicade, a clinically used anti-TNFalpha antibody, small interfering RNA (siRNA) against p50 and p65 nuclear factor-kappaB (NF-kappaB) isoforms, curcumin, a well characterized natural NF-kappaB inhibitor, as well as a dominant negative inhibitor of kappaB alpha (IkappaBalpha), prevented GGT activation at various levels, illustrating the involvement of this signaling pathway in TNFalpha-induced stimulation. Over-expression of receptor of TNFalpha-1 (TNFR1), TNFR-associated factor-2 (TRAF2), TNFR-1 associated death domain (TRADD), dominant negative (DN) IkappaBalpha or NF-kappaB p65 further confirmed GGT promoter activation via NF-kappaB. Linker insertion mutagenesis of 536 bp of the proximal GGT promoter revealed NF-kappaB and Sp1 binding sites at -110 and -78 relative to the transcription start site, responsible for basal GGT transcription. Mutation of the NF-kappaB site located at -110 additionally inhibited TNFalpha-induced promoter induction. Chromatin immunoprecipitation (ChIP) assays confirmed mutagenesis results and further demonstrated that TNFalpha treatment induced in vivo binding of both NF-kappaB and Sp1, explaining increased GGT expression, and led to RNA polymerase II recruitment under inflammatory conditions. [less ▲]

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