ArticlePLoS genetics2016
A RUNX2-Mediated Epigenetic Regulation of the Survival of p53 Defective Cancer Cells.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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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.
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Who cites it
36 citing papers in PubMed, 45 citations in OpenAlex.
- RUNX2 influences alternative splicing of genes associated with gastric cancer progression by regulating SF3B6 expression in HGC-27 cells.Molecular genetics and genomics : MGG · 2026Article
- Gene Targeted Therapies for Neurodegenerative Disorders: Strategies and Implications in ALS and SMA.Genes · 2026Review
- Genetic and pharmaceutical manipulation of H3K9 methyltransferase Suv39h1 promotes liver regeneration by unleashing HMGB2 transcription.Experimental & molecular medicine · 2026Article
- VHL synthetic lethality screens uncover CBF-β as a negative regulator of STING.Nature communications · 2026Article
- Menin-MLL inhibitors as a new therapeutic target for middle ear cholesteatoma.Scientific reports · 2026Article
- Epigenetic Regulation of RUNX2 in Bone Mechanobiology.Results and problems in cell differentiation · 2026Review
- Menin inhibitor MI-503 exhibits potent anti-cancer activity in osteosarcoma.Scientific reports · 2025Article
- Identification and partial characterization of new cell density-dependent nucleocytoplasmic shuttling proteins and open chromatin.Scientific reports · 2023Article
- C/ebpα represses the oncogenic Runx3-Myc axis in p53-deficient osteosarcoma development.Oncogene · 2023Article
- SOX9 is a key component of RUNX2-regulated transcriptional circuitry in osteosarcoma.Cell & bioscience · 2023Article
- Review
- Review
- Circular RNA hsa_circ_001350 contributes to osteosarcoma progression by regulating microRNA-578/CCR4-NOT transcription complex and subunit 7/Wnt signaling.American journal of cancer research · 2023Article
- Cellular dynamics of distinct skeletal cells and the development of osteosarcoma.Frontiers in endocrinology · 2023Review
- Menin Enhances Androgen Receptor-Independent Proliferation and Migration of Prostate Cancer Cells.Molecules and cells · 2022Article
- Article
- Fatty acid oxidation is required for embryonic stem cell survival during metabolic stress.EMBO reports · 2021Article
- CBFB cooperates with p53 to maintain TAp73 expression and suppress breast cancer.PLoS genetics · 2021Article
- Current developments of targeting the p53 signaling pathway for cancer treatment.Pharmacology & therapeutics · 2021Review
- Use of signals of positive and negative selection to distinguish cancer genes and passenger genes.eLife · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
The inactivation of p53 creates a major challenge for inducing apoptosis in cancer cells. An attractive strategy is to identify and subsequently target the survival signals in p53 defective cancer cells. Here we uncover a RUNX2-mediated survival signal in p53 defective cancer cells. The inhibition of this signal induces apoptosis in cancer cells but not non-transformed cells. Using the CRISPR technology, we demonstrate that p53 loss enhances the apoptosis caused by RUNX2 knockdown. Mechanistically, RUNX2 provides the survival signal partially through inducing MYC transcription. Cancer cells have high levels of activating histone marks on the MYC locus and concomitant high MYC expression. RUNX2 knockdown decreases the levels of these histone modifications and the recruitment of the Menin/MLL1 (mixed lineage leukemia 1) complex to the MYC locus. Two inhibitors of the Menin/MLL1 complex induce apoptosis in p53 defective cancer cells. Together, we identify a RUNX2-mediated epigenetic mechanism of the survival of p53 defective cancer cells and provide a proof-of-principle that the inhibition of this epigenetic axis is a promising strategy to kill p53 defective cancer cells.
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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.