Chromatin-modifying agents in anti-cancer therapy

Seidel, Carole; Florean, Cristina; Schnekenburger, Michaël; Dicato, Mario; Diederich, Marc

doi:10.1016/j.biochi.2012.05.012

Cited by 71 publications

(73 citation statements)

References 209 publications

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“…Widely used in epigenetic anticancer treatments (Jones and Taylor 1980;Seidel et al 2012;Yang et al 2014), 5-aza-dC is a hypomethylating agent that works by inhibiting DNA methyltransferase activity (Creusot et al 1982;Christman 2002). During continued exposure, 5-aza-dC molecules are incorporated into DNA during replication in the place of cytosine.…”

Section: Methodsmentioning

confidence: 99%

DNA Methylation and Sex Allocation in the Parasitoid WaspNasonia vitripennis

Cook

Pannebakker

Tauber

et al. 2015

The American Naturalist

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Dryad data: http://dx.doi.org/10.5061/dryad.15nj0. abstract:The role of epigenetics in the control and evolution of behavior is being increasingly recognized. Here we test whether DNA methylation influences patterns of adaptive sex allocation in the parasitoid wasp Nasonia vitripennis. Female N. vitripennis allocate offspring sex broadly in line with local mate competition (LMC) theory. However, recent theory has highlighted how genomic conflict may influence sex allocation under LMC, conflict that requires parentof-origin information to be retained by alleles through some form of epigenetic signal. We manipulated whole-genome DNA methylation in N. vitripennis females using the hypomethylating agent 5-aza-2 0 -deoxycytidine. Across two replicated experiments, we show that disruption of DNA methylation does not ablate the facultative sex allocation response of females, as sex ratios still vary with cofoundress number as in the classical theory. However, sex ratios are generally shifted upward when DNA methylation is disrupted. Our data are consistent with predictions from genomic conflict over sex allocation theory and suggest that sex ratios may be closer to the optimum for maternally inherited alleles.

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Section: Methodsmentioning

confidence: 99%

DNA Methylation and Sex Allocation in the Parasitoid WaspNasonia vitripennis

Cook

Pannebakker

Tauber

et al. 2015

The American Naturalist

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“…As both parasites and cancer capture environmental signals to modulate adaptations, the study of kinases is relevant for our understanding of host parasite/cancer interactions. Histonemodifying enzymes (HMEs) have also been intensively studied for drug development in cancer and parasitic diseases [3][4][5] . HMEs regulate epigenetic modifications of chromatin (reviewed 6 ).…”

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confidence: 99%

Cancer and parasitic infections: similarities and opportunities for the development of new control tools

Oliveira

2014

Rev. Soc. Bras. Med. Trop.

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Lifestyle similarities between parasites and cancer have inspired parasitologists to use approaches analogous to those used in oncology and to explore the interface between these fields. The similarities have not escaped the notice of oncologists. Cancer may be thought of as a developing species that behaves in a manner akin to parasites 1 . Both are autonomous and not subjected to regular signaling mechanisms, although they make use of signals and resources for their own benefit. In parasitology, research approaches inspired or enabled by cancer research have been used in the design of new antiparasitic drugs. For example, in schistosomiasis, imatinib, a drug used to treat chronic myelogenous leukemia (CML), has been found to produce a substantial effect on parasite physiology in vitro 2 . Examples of the use of kinases as drug targets can also be found in the literature for malaria and leishmaniasis, among others. Parasitic kinomes are also of interest, as kinases are key transducers of environmental signals and trigger physiological adaptations in the parasite. As both parasites and cancer capture environmental signals to modulate adaptations, the study of kinases is relevant for our understanding of host parasite/cancer interactions. Histonemodifying enzymes (HMEs) have also been intensively studied for drug development in cancer and parasitic diseases [3][4][5] . HMEs regulate epigenetic modifications of chromatin (reviewed 6 ).Epigenetic modifications mediate sequence-independent transcriptional regulation. Such modifications include DNA methylation or the alteration of histone proteins in a particular region. Histone modifications such as methylation or acetylation alter heterochromatin status, thereby regulating genes in the region. HMEs, specifically histone deacetylases (HDACs), are good antiparasitic targets; the drug suberanilohydroxamic acid (SAHA) inhibits parasite enzymatic activity. Active compounds have been developed to target the histone deacetylases of Plasmodium sp., Schistosoma mansoni, and other species 7,8 . A compound named SB939, a pan-HDAC inhibitor acting on class I, II, and IV HDACs, was found to inhibit asexual growth of Plasmodium in human erythrocytes and exoerythrocytic-stage parasites in human hepatocytes 7 . A structure-based approach was used to develop several small molecule inhibitors of the S. mansoni enzyme smHDA8 8 (Figure 1), thus reducing parasite survival. Recently, a consortium was established to develop

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“…The quercetin flavonoids are capable to act as anti-inflammatory agents via modulation of pro-inflammatory gene expression and signal transduction pathways (Tuñón,et al,2009). Activated NF-κBp65 (RelA) and the aberrant HDAC activity play the pivotal role of tumorigenesis (Sun et al, 2012;Seidel et al, 2012). Additionally there is link between RelA/p65 and class I HDACs in nuclear translocation as well as RelA/p65 DNA binding activity (Lehmann, et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Anti-CSC Effects in Human Esophageal Squamous Cell Carcinomas and Eca109/9706 Cells Induced by Nanoliposomal Quercetin Alone or Combined with CD 133 Antiserum

Naigang¹,

Mo²,

Li³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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CD133 was recently reported to be a cancer stem cell and prognostic marker. Quercetin is considered as a potential chemopreventive agent due to its involvement in suppression of oxidative stress, proliferation and metastasis. In this study, the expression of CD133/CD44 in esophageal carcinomas and Eca109/9706 cells was explored. In immunoflurorescence the locations of CD133 + and multidrug resistance 1 (MDR 1) + in the same E-cancer cells were coincident, mainly in cytomembranes. In esophageal squamous cell carcinomas detected by double/single immunocytochemistry, small CD133 + cells were located in the basal layer of stratified squamous epithelium, determined as CSLC (cancer stem like cells); CD44 + surrounding the cells appeared in diffuse pattern, and the larger CD44 + (hi) cells were mainly located in the prickle cell layer of the epithelium, as progenitor cells. In E-cancer cells exposed to nanoliposomal quercetin (nLQ with cytomembrane permeability), down-regulation of NF-κBp65, histone deacetylase 1 (HDAC1) and cyclin D1 and up-regulation of caspase-3 were shown by immunoblotting, and attenuated HDAC1 with nuclear translocation and promoted E-cadherin expression were demonstrated by immunocytochemistry. In particular, enhanced E-cadherin expression reflected the reversed epithelial mesenchymal transition (EMT) capacity of nLQ, acting as cancer attenuator/preventive agent. nLQ acting as an HDAC inhibitor induced apoptotic cells detected by TUNEL assay mediated via HDAC-NF-κB signaling. Apoptotic effects of liposomal quercetin (LQ, with cytomembrane-philia) combined with CD133 antiserum were also detected by CD133 immunocytochemistry combined with TUNEL assay. The combination could induce greater apoptotic effects than nLQ induced alone, suggesting a novel anti-CSC treatment strategy.

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Chromatin-modifying agents in anti-cancer therapy

Cited by 71 publications

References 209 publications

DNA Methylation and Sex Allocation in the Parasitoid WaspNasonia vitripennis

DNA Methylation and Sex Allocation in the Parasitoid WaspNasonia vitripennis

Cancer and parasitic infections: similarities and opportunities for the development of new control tools

Anti-CSC Effects in Human Esophageal Squamous Cell Carcinomas and Eca109/9706 Cells Induced by Nanoliposomal Quercetin Alone or Combined with CD 133 Antiserum

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