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dc.contributor.authorDemetriadou, Christinaen
dc.contributor.authorPavlou, Demetriaen
dc.contributor.authorMpekris, Fotiosen
dc.contributor.authorAchilleos, Charisen
dc.contributor.authorStylianopoulos, Triantafyllosen
dc.contributor.authorZaravinos, Apostolosen
dc.contributor.authorPapageorgis, Panagiotisen
dc.contributor.authorKirmizis, Antonisen
dc.creatorDemetriadou, Christinaen
dc.creatorPavlou, Demetriaen
dc.creatorMpekris, Fotiosen
dc.creatorAchilleos, Charisen
dc.creatorStylianopoulos, Triantafyllosen
dc.creatorZaravinos, Apostolosen
dc.creatorPapageorgis, Panagiotisen
dc.creatorKirmizis, Antonisen
dc.date.accessioned2021-01-27T10:17:22Z
dc.date.available2021-01-27T10:17:22Z
dc.date.issued2019
dc.identifier.issn2041-4889
dc.identifier.urihttp://gnosis.library.ucy.ac.cy/handle/7/63665
dc.description.abstractN-alpha-acetyltransferase 40 (NAA40) catalyzes the transfer of an acetyl moiety to the alpha-amino group of serine 1 (S1) on histones H4 and H2A. Our previous studies linked NAA40 and its corresponding N-terminal acetylation of histone H4 (N-acH4) to colorectal cancer (CRC). However, the role of NAA40 in CRC development was not investigated. Here, we show that NAA40 protein and mRNA levels are commonly increased in CRC primary tissues compared to non-malignant specimens. Importantly, depletion of NAA40 inhibits cell proliferation and survival of CRC cell lines and increases their sensitivity to 5-Fluorouracil (5-FU) treatment. Moreover, the absence of NAA40 significantly delays the growth of human CRC xenograft tumors. Intriguingly, we found that NAA40 knockdown and loss of N-acH4 reduce the levels of symmetric dimethylation of histone H4 (H4R3me2s) through transcriptional downregulation of protein arginine methyltransferase 5 (PRMT5). NAA40 depletion and subsequent repression of PRMT5 results in altered expression of key oncogenes and tumor suppressor genes leading to inhibition of CRC cell growth. Consistent with this, NAA40 mRNA levels correlate with those of PRMT5 in CRC patient tissues. Taken together, our results establish the oncogenic function of the epigenetic enzyme NAA40 in colon cancer and support its potential as a therapeutic target.en
dc.language.isoenen
dc.sourceCell Death & Diseaseen
dc.source.urihttps://www.nature.com/articles/s41419-019-1487-3
dc.titleNAA40 contributes to colorectal cancer growth by controlling PRMT5 expressionen
dc.typeinfo:eu-repo/semantics/article
dc.identifier.doi10.1038/s41419-019-1487-3
dc.description.volume10
dc.description.issue3
dc.description.startingpage1
dc.description.endingpage14
dc.author.facultyΠολυτεχνική Σχολή / Faculty of Engineering
dc.author.departmentΤμήμα Μηχανικών Μηχανολογίας και Κατασκευαστικής / Department of Mechanical and Manufacturing Engineering
dc.type.uhtypeArticleen
dc.contributor.orcidStylianopoulos, Triantafyllos [0000-0002-3093-1696]
dc.contributor.orcidKirmizis, Antonis [0000-0002-3748-8711]
dc.contributor.orcidMpekris, Fotios [0000-0002-7125-4062]
dc.contributor.orcidAchilleos, Charis [0000-0002-1116-7733]
dc.contributor.orcidZaravinos, Apostolos [0000-0003-4625-5562]
dc.contributor.orcidPapageorgis, Panagiotis [0000-0002-7595-5616]
dc.gnosis.orcid0000-0002-3093-1696
dc.gnosis.orcid0000-0002-3748-8711
dc.gnosis.orcid0000-0002-7125-4062
dc.gnosis.orcid0000-0002-1116-7733
dc.gnosis.orcid0000-0003-4625-5562
dc.gnosis.orcid0000-0002-7595-5616


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