Evidence map›Paper›PMID 21347396›Full record

ArticlePloS one2011

RNAi-mediated knock-down of arylamine N-acetyltransferase-1 expression induces E-cadherin up-regulation and cell-cell contact growth inhibition.

Jacky M Tiang, Neville J Butcher, Carleen Cullinane, Patrick O Humbert, Rodney F Minchin

Abstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Upregulation of cytidine deaminase in NAT1 knockout breast cancer cells.Journal of cancer research and clinical oncology · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Proteomic analysis of arylamineToxicology reports · 2022
    Article
  13. ArylamineFrontiers in pharmacology · 2022
    Article
  14. Human ArylamineFrontiers in pharmacology · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. EMBO reports · 2019
    Article
  20. Journal of oncology · 2019
    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

5 authors.

Jacky M TiangSchool of Biomedical Sciences, University of Queensland, St. Lucia, Queensland, Australia.
Neville J Butcher
Carleen Cullinane
Patrick O Humbert
Rodney F Minchin

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arylamine N-acetyltransferase-1 (NAT1) is an enzyme that catalyzes the biotransformation of arylamine and hydrazine substrates. It also has a role in the catabolism of the folate metabolite p-aminobenzoyl glutamate. Recent bioinformatics studies have correlated NAT1 expression with various cancer subtypes. However, a direct role for NAT1 in cell biology has not been established. In this study, we have knocked down NAT1 in the colon adenocarcinoma cell-line HT-29 and found a marked change in cell morphology that was accompanied by an increase in cell-cell contact growth inhibition and a loss of cell viability at confluence. NAT1 knock-down also led to attenuation in anchorage independent growth in soft agar. Loss of NAT1 led to the up-regulation of E-cadherin mRNA and protein levels. This change in E-cadherin was not attributed to RNAi off-target effects and was also observed in the prostate cancer cell-line 22Rv1. In vivo, NAT1 knock-down cells grew with a longer doubling time compared to cells stably transfected with a scrambled RNAi or to parental HT-29 cells. This study has shown that NAT1 affects cell growth and morphology. In addition, it suggests that NAT1 may be a novel drug target for cancer therapeutics.

Indexed as

Gene Knockdown TechniquesRNA InterferenceAnimalsArylamine N-AcetyltransferaseCadherinsCell CommunicationCell ProliferationCell SurvivalColonic NeoplasmsFemaleHT29 CellsHumansIsoenzymesKineticsMiceRNA, MessengerArylamine N-AcetyltransferaseCadherinsIsoenzymesN-acetyltransferase 1RNA, MessengerRNA, Small Interfering

Identifiers

PMID21347396
PMCPMC3036737

What OpenQuestion holds

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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.