Targeting epigenetic mechanisms and microRNAs by aspirin and other non steroidal anti-inflammatory agents-implications for cancer treatment and chemoprevention

dc.contributor.author	Γιαννακοπούλου, Ευγενία Χ.	el
dc.date.accessioned	2015-06-10T14:04:32Z
dc.date.available	2015-06-10T14:04:32Z
dc.date.issued	2015-06-10
dc.identifier.uri	http://hdl.handle.net/11400/15639
dc.rights	Αναφορά Δημιουργού-Μη Εμπορική Χρήση-Όχι Παράγωγα Έργα 3.0 Ηνωμένες Πολιτείες	*
dc.rights.uri	http://creativecommons.org/licenses/by-nc-nd/3.0/us/	*
dc.source	http://link.springer.com/article/10.1007%2Fs13402-014-0175-7	en
dc.subject	Μεθυλίωση του DNA
dc.subject	επιδράσεις των φαρμάκων
dc.subject	ρύθμιση της γονιδιακής έκφρασης
dc.subject	ενετικά επιγένεσης
dc.subject	γενετική
dc.subject	Νεοπλάσματα
dc.subject	DNA methylation
dc.subject	Effect of drugs on
dc.subject	gene expression regulation
dc.subject	genetic epigenesis
dc.subject	genetics
dc.subject	neoplasms
dc.title	Targeting epigenetic mechanisms and microRNAs by aspirin and other non steroidal anti-inflammatory agents-implications for cancer treatment and chemoprevention	en
heal.type	journalArticle
heal.classification	Ογκολογία
heal.classification	Καρκίνος
heal.classification	Oncology
heal.classification	Cancer
heal.classificationURI	N/A-Ογκολογία
heal.classificationURI	N/A-Καρκίνος
heal.classificationURI	http://id.loc.gov/authorities/subjects/sh85094724
heal.classificationURI	http://zbw.eu/stw/descriptor/18899-3
heal.keywordURI	http://lod.nal.usda.gov/34172
heal.keywordURI	http://id.loc.gov/authorities/subjects/sh00004603
heal.keywordURI	http://lod.nal.usda.gov/14043
heal.keywordURI	http://lod.nal.usda.gov/702
heal.identifier.secondary	DOI: 10.1007/s13402-014-0175-7
heal.language	en
heal.access	campus
heal.recordProvider	Τεχνολογικό Εκπαιδευτικό Ίδρυμα Αθήνας. Σχολή Επαγγελμάτων Υγείας και Πρόνοιας. Τμήμα Ιατρικών Εργαστηρίων	el
heal.publicationDate	2014-06-01
heal.bibliographicCitation	Yiannakopoulou, E. (2014) Targeting epigenetic mechanisms and microRNAs by aspirin and other non steroidal anti-inflammatory agents-implications for cancer treatment and chemoprevention. Cellular oncology (Dordrecht). [Online] 37 (3), pp.167-178. Available from: http://link.springer.com [Accessed 10/06/2015]	en
heal.abstract	BACKGROUND: Epigenetic processes and miRNAs have been recognized as new targets for anticancer drug design. However, old multi-target drugs such as aspirin may also target epigenetic processes. AIM: This review aims to provide an overview of our current knowledge on the modulation of epigenetic processes by aspirin and other non steroidal anti-inflammatory agents (NSAIDs) and their implications for cancer treatment and chemoprevention. SYNTHESIS: In vitro and in vivo studies, as well as primary patient data, suggest that aspirin and other NSAIDs reverse tumour suppressor gene hypermethylation in cancer tissues. It must be emphasized that, at this point in time, patient data are limited and DNA hypermethylation reversal has been investigated, but not tumour suppressor gene activation. In addition, evidence from experimental and patient data suggests that aspirin and NSAIDs may also reverse global DNA hypomethylation. At the histone level, both induction and inhibition of deacetylases by aspirin have been reported. Also, direct acetylation of histones by aspirin has been reported, while the natural salicylate anacardic acid has been found to inhibit histone acetyltransferase p300 both in vitro and in vivo, and to regulate gene expression through modulation of histone acetylation. Salicylates and other NSAIDs may also down-regulate miRNAs with oncogene-like functions or up-regulate miRNAs with tumour suppressor-like functions. Up till now, clinical trials have been aimed at investigating the effect of salicylates and NSAIDs on a limited number of miRNAs. CONCLUSION: So, although the existing evidence is still limited, evidence is accumulating that epigenetic targets may represent nodal targets for the anti-proliferative actions of salicylates and NSAIDs. This, in turn, may have implications for cancer chemoprevention and treatment. Undoubtedly, this notion requires further investigation, but if proved correct, it could lead to the design of less toxic agents that target epigenetic processes as part of existing or novel multi-targeted treatment modalities.	en
heal.publisher	Springer Netherlands	en
heal.journalName	Cellular oncology (Dordrecht)	en
heal.journalType	peer-reviewed
heal.fullTextAvailability	false