Evidence map›Paper›PMID 30535344›Full record

ReviewJournal of molecular cell biology2019

Functional relationship between p53 and RUNX proteins.

Suk-Chul Bae, Arun Mouli Kolinjivadi, Yoshiaki Ito

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of molecular cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Cells · 2023
    Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Intracranial Aneurysms Induced byFrontiers in neurology · 2022
    Article
  10. Article
  11. Article
  12. Review
  13. Epigenetic priming sensitizes gastric cancer cells to irinotecan and cisplatin by restoring multiple pathways.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2020
    Article
  14. Review
  15. p53: updates on mechanisms, biology and therapy (I).Journal of molecular cell biology · 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

3 authors at 2 institutions in 2 countries.

Suk-Chul BaeDepartment of Biochemistry, School of Medicine, and Institute for Tumour Research, Chungbuk National University, Cheongju, South Korea.
Arun Mouli KolinjivadiCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Yoshiaki ItoCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
National University of Singapore · SGChungbuk National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RUNX genes belong to a three-membered family of transcription factors, which are well established as master regulators of development. Of them, aberrations in RUNX3 expression are frequently observed in human malignancies primarily due to epigenetic silencing, which is often overlooked. At the G1 phase of the cell cycle, RUNX3 regulates the restriction (R)-point, a mechanism that decides cell cycle entry. Deregulation at the R-point or loss of RUNX3 results in premature entry into S phase, leading to a proliferative advantage. Inactivation of Runx1 and Runx2 induce immortalization of mouse embryo fibroblast. As a consequence, RUNX loss induces pre-cancerous lesions independent of oncogene activation. p53 is the most extensively studied tumour suppressor. p53 plays an important role to prevent tumour progression but not tumour initiation. Therefore, upon oncogene activation, early inactivation of RUNX genes and subsequent mutation of p53 appear to result in tumour initiation and progression. Recently, transcription-independent DNA repairing roles of RUNX3 and p53 are emerging. Being evolutionarily old genes, it appears that the primordial function of p53 is to protect genome integrity, a function that likely extends to the RUNX gene as well. In this review, we examine the mechanism and sequence of actions of these tumour suppressors in detail.

Indexed as

AnimalsCell Transformation, NeoplasticCore Binding Factor Alpha 1 SubunitCore Binding Factor Alpha 2 SubunitCore Binding Factor Alpha 3 SubunitCore Binding Factor alpha SubunitsDNA-Binding ProteinsHumansTumor Suppressor Protein p53Core Binding Factor Alpha 1 SubunitCore Binding Factor Alpha 2 SubunitCore Binding Factor Alpha 3 SubunitCore Binding Factor alpha SubunitsDNA-Binding ProteinsTumor Suppressor Protein p53p53RUNXtumour suppressor

Identifiers

PMID30535344
PMCPMC6478125
OpenAlexW2904978480

What OpenQuestion holds

Textmetadata
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.