Evidence map›Paper›PMID 27535933›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Lysine methylation represses p53 activity in teratocarcinoma cancer cells.

Jiajun Zhu, Zhixun Dou, Morgan A Sammons, Arnold J Levine, Shelley L Berger

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. The role and application prospects of ANXA1 in gastric cancer cells.Medical oncology (Northwood, London, England) · 2025
    Review
  5. Review
  6. Review
  7. Lysine and arginine methylation of transcription factors.Cellular and molecular life sciences : CMLS · 2024
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. The Enigmatic Role of TP53 in Germ Cell Tumours: Are We Missing Something?International journal of molecular sciences · 2021
    Review
  16. Article
  17. Article
  18. The Basally Expressed p53-Mediated Homeostatic Function.Frontiers in cell and developmental biology · 2021
    Review
  19. 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

5 authors at 2 institutions in 1 country.

Jiajun ZhuEpigenetics Program, Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104; Biomedical Graduate Studies, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104;
Zhixun DouEpigenetics Program, Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104;
Morgan A SammonsEpigenetics Program, Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104;
Arnold J LevineThe Simons Center for Systems Biology, School of Natural Sciences, Institute for Advanced Study, Princeton, NJ 08540 alevine@ias.edu bergers@upenn.edu.
Shelley L BergerEpigenetics Program, Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104; alevine@ias.edu bergers@upenn.edu.
University of Pennsylvania · USCenter for Systems Biology · US

Funding

Role of PCAF/GCN5 Acetylation on p53 TransactivationR01CA078831 · NCI · WISTAR INSTITUTE · PI BERGER, SHELLEY L · 1999 to 2022
$7.8M
NCI NIH HHS R01 CA078831
6 · The paper itself

Abstract

TP53 (which encodes the p53 protein) is the most frequently mutated gene among all human cancers, whereas tumors that retain the wild-type TP53 gene often use alternative mechanisms to repress the p53 tumor-suppressive function. Testicular teratocarcinoma cells rarely contain mutations in TP53, yet the transcriptional activity of wild-type p53 is compromised, despite its high expression level. Here we report that in the teratocarcinoma cell line NTera2, p53 is subject to lysine methylation at its carboxyl terminus, which has been shown to repress p53's transcriptional activity. We show that reduction of the cognate methyltransferases reactivates p53 and promotes differentiation of the NTera2 cells. Furthermore, reconstitution of methylation-deficient p53 mutants into p53-depleted NTera2 cells results in elevated expression of p53 downstream targets and precocious loss of pluripotent gene expression compared with re-expression of wild-type p53. Our results provide evidence that lysine methylation of endogenous wild-type p53 represses its activity in cancer cells and suggest new therapeutic possibilities of targeting testicular teratocarcinoma.

Indexed as

Gene Expression Regulation, NeoplasticProtein Processing, Post-TranslationalCell DifferentiationCell Line, TumorCell ProliferationHistone-Lysine N-MethyltransferaseHumansLysineMaleMethylationProtein DomainsRNA, Small InterferingSignal TransductionTeratocarcinomaTesticular NeoplasmsTumor Suppressor Protein p53Histone-Lysine N-MethyltransferaseKMT5A protein, humanLysineRNA, Small InterferingSMYD2 protein, humanTumor Suppressor Protein p53cancermethylationp53pluripotencyteratocarcinoma

Identifiers

PMID27535933
PMCPMC5024588
OpenAlexW2515201209

What OpenQuestion holds

Textmetadata
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.