ReviewInternational journal of genomics2013
RUNX Family Participates in the Regulation of p53-Dependent DNA Damage Response.
Review in International journal of genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 4 of them syntheses that pooled it.
What it found
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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.
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.
Who cites it
30 citing papers in PubMed, 4 syntheses or guidelines pooled it, 51 citations in OpenAlex.
- An early biomarker and potential therapeutic target of RUNX 3 hypermethylation in breast cancer, a system review and meta-analysis.Oncotarget · 2017Pooled it
- Clinicopathological significance and potential drug target of RUNX3 in non-small cell lung cancer: a meta-analysis.Drug design, development and therapy · 2015Pooled it
- Clinicopathological significance of RUNX3 gene hypermethylation in hepatocellular carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- Clinicopathological significance and potential drug target of RUNX3 in breast cancer.Drug design, development and therapy · 2014Pooled it
- DNA methylation changes in thyroid cancer patients infected with SARS-CoV-2.Updates in surgery · 2026Article
- Rapid Screening to Identify Antivirals against Persistent and Acute Coxsackievirus B3 Infection.ACS infectious diseases · 2024Article
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- A RUNX-targeted gene switch-off approach modulates the BIRC5/PIF1-p21 pathway and reduces glioblastoma growth in mice.Communications biology · 2022Article
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- Article
- Oncogenic RUNX3: A Link between p53 Deficiency and MYC Dysregulation.Molecules and cells · 2020Review
- Role of RUNX Family Transcription Factors in DNA Damage Response.Molecules and cells · 2020Review
- SET7/9 promotes multiple malignant processes in breast cancer development via RUNX2 activation and is negatively regulated by TRIM21.Cell death & disease · 2020Article
- Methylation-regulated ZNF545 inhibits growth of the p53-mutant KYSE150 cell line by inducing p21 and Bax.Experimental and therapeutic medicine · 2019Article
- Epigenetic inactivation ofAnnals of surgical treatment and research · 2018Article
- Identification of a p53 target, CD137L, that mediates growth suppression and immune response of osteosarcoma cells.Scientific reports · 2017Article
- MiR-23a targets RUNX2 and suppresses ginsenoside Rg1-induced angiogenesis in endothelial cells.Oncotarget · 2017Article
- Genetic regulation of the RUNX transcription factor family has antitumor effects.The Journal of clinical investigation · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A proper DNA damage response (DDR), which monitors and maintains the genomic integrity, has been considered to be a critical barrier against genetic alterations to prevent tumor initiation and progression. The representative tumor suppressor p53 plays an important role in the regulation of DNA damage response. When cells receive DNA damage, p53 is quickly activated and induces cell cycle arrest and/or apoptotic cell death through transactivating its target genes implicated in the promotion of cell cycle arrest and/or apoptotic cell death such as p21(WAF1) , BAX, and PUMA. Accumulating evidence strongly suggests that DNA damage-mediated activation as well as induction of p53 is regulated by posttranslational modifications and also by protein-protein interaction. Loss of p53 activity confers growth advantage and ensures survival in cancer cells by inhibiting apoptotic response required for tumor suppression. RUNX family, which is composed of RUNX1, RUNX2, and RUNX3, is a sequence-specific transcription factor and is closely involved in a variety of cellular processes including development, differentiation, and/or tumorigenesis. In this review, we describe a background of p53 and a functional collaboration between p53 and RUNX family in response to DNA damage.
Identifiers
What OpenQuestion holds
Registered trials
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.