Evidence map›Paper›PMID 30858358›Full record

ArticleCell death & disease2019

NAA40 contributes to colorectal cancer growth by controlling PRMT5 expression.

Christina Demetriadou, Demetria Pavlou, Fotios Mpekris, Charis Achilleos, Triantafyllos Stylianopoulos, Apostolos Zaravinos, Panagiotis Papageorgis, Antonis Kirmizis

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
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  12. Review
  13. Article
  14. Article
  15. Role of PRMT1 and PRMT5 in Breast Cancer.International journal of molecular sciences · 2024
    Review
  16. Article
  17. Article
  18. Article
  19. Impact of Protein NLife (Basel, Switzerland) · 2023
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Christina DemetriadouEpigenetics Laboratory, Department of Biological Sciences, University of Cyprus, 2109, Nicosia, Cyprus.
Demetria PavlouEpigenetics Laboratory, Department of Biological Sciences, University of Cyprus, 2109, Nicosia, Cyprus.
Fotios MpekrisCancer Biophysics Laboratory, Department of Mechanical and Manufacturing Engineering, University of Cyprus, 1678, Nicosia, Cyprus.
Charis AchilleosTumor Viruses and Cancer Laboratory, Department of Biological Sciences, University of Cyprus, 2109, Nicosia, Cyprus.
Triantafyllos StylianopoulosCancer Biophysics Laboratory, Department of Mechanical and Manufacturing Engineering, University of Cyprus, 1678, Nicosia, Cyprus.
Apostolos ZaravinosDepartment of Life Sciences, European University Cyprus, 1516, Nicosia, Cyprus.ORCID http://orcid.org/0000-0003-4625-5562
Panagiotis PapageorgisDepartment of Life Sciences, European University Cyprus, 1516, Nicosia, Cyprus.
Antonis KirmizisEpigenetics Laboratory, Department of Biological Sciences, University of Cyprus, 2109, Nicosia, Cyprus. kirmizis@ucy.ac.cy.ORCID http://orcid.org/0000-0002-3748-8711
University of Cyprus · CYEuropean University Cyprus · CY

Funding

European Research Council 260797
6 · The paper itself

Abstract

N-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.

Indexed as

AcetylationAdenocarcinomaAnimalsCell Line, TumorCell ProliferationCell SurvivalColorectal NeoplasmsGene Expression Regulation, NeoplasticHCT116 CellsHistonesHT29 CellsHumansMaleMethylationMiceMice, NudeHistonesNAA40 protein, humanN-Terminal Acetyltransferase DPRMT5 protein, humanProtein-Arginine N-Methyltransferases

Identifiers

PMID30858358
PMCPMC6411749
OpenAlexW2922016296

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.