Evidence map›Paper›PMID 27270439›Full record

ArticleOncogene2017

Lysine demethylase KDM3A regulates breast cancer cell invasion and apoptosis by targeting histone and the non-histone protein p53.

S Ramadoss, G Guo, C-Y Wang

Abstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

67 citing papers in PubMed, 103 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Discovery and structural studies of histone demethylases.Frontiers in epigenetics and epigenomics · 2025
    Review
  10. Lysine and arginine methylation of transcription factors.Cellular and molecular life sciences : CMLS · 2024
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Targeting epigenetic regulators to overcome drug resistance in cancers.Signal transduction and targeted therapy · 2023
    Review
  17. Article
  18. Article
  19. Article
  20. Article

7 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

S RamadossLaboratory of Molecular Signaling, Division of Oral Biology and Medicine, School of Dentistry and Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, CA, USA.
G GuoLaboratory of Molecular Signaling, Division of Oral Biology and Medicine, School of Dentistry and Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, CA, USA.
C-Y WangLaboratory of Molecular Signaling, Division of Oral Biology and Medicine, School of Dentistry and Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, CA, USA.
UCLA Jonsson Comprehensive Cancer CenterSamueli Institute · US

Funding

Molecular and Genetic Determinants of Invasion in HNSCCR01DE015964 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WANG, CUN-YU · 2004 to 2019
$6.6M
PS-341-induced Apoptosis in Squamous Cell CarcinomaR37DE013848 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WANG, CUN-YU · 2006 to 2015
$3.5M
Epigenetic Control of HPV-associated Oral CarcinogenesisR01DE023874 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KIM, REUBEN HAN-KYU, WANG, CUN-YU · 2013 to 2017
$2.3M
NIDCR NIH HHS R01 DE015964NIDCR NIH HHS R01 DE023874NIDCR NIH HHS R37 DE013848
6 · The paper itself

Abstract

Invasive growth and apoptosis resistance of breast cancer cells are associated with metastasis and disease relapse. Here we identified that the lysine-specific demethylase KDM3A played a dual role in breast cancer cell invasion and apoptosis by demethylating histone and the non-histone protein p53, respectively. While inducing pro-invasive genes by erasing repressive histone H3 lysine 9 methylation, KDM3A promotes chemoresistance by demethylating p53. KDM3A suppressed pro-apoptotic functions of p53 by erasing p53-K372me1, as this methylation is crucial for the stability of chromatin-bound p53. Unexpectedly, depletion of KDM3A was capable of reactivating mutated p53 to induce the expression of pro-apoptotic genes in breast cancer with mutant p53. Moreover, KDM3A knockdown also potently inhibited tumorigenic potentials of breast cancer stem-like cells and rendered them sensitive to apoptosis induced by chemotherapeutic drugs. Taken together, our results suggest that KDM3A might be a potential therapeutic target for human breast cancer treatment and prevention.

Indexed as

ApoptosisAnimalsAntineoplastic AgentsApoptosis Regulatory ProteinsBreast NeoplasmsCell Line, TumorCell MovementDisease Models, AnimalDrug Resistance, NeoplasmEpigenesis, GeneticFemaleGene ExpressionGene Knockdown TechniquesHistonesHumansJumonji Domain-Containing Histone DemethylasesAntineoplastic AgentsApoptosis Regulatory ProteinsBBC3 protein, humanHistonesJumonji Domain-Containing Histone DemethylasesKDM3A protein, humanLysinePMAIP1 protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Tumor Suppressor Protein p53

Identifiers

PMID27270439
PMCPMC5140781
OpenAlexW2462738515

What OpenQuestion holds

Textmetadata
LicenceTDM
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.