ArticleOncotarget2014
AP4 is required for mitogen- and c-MYC-induced cell cycle progression.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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
14 citing papers in PubMed, 20 citations in OpenAlex.
- Transcription factor activator protein 4 (AP4)-mediated intrinsic control of axon regeneration.Science advances · 2025Article
- Article
- The MITF regulatory network in melanoma.Pigment cell & melanoma research · 2022Article
- AP4 suppresses DNA damage, chromosomal instability and senescence via inducing MDC1/Mediator of DNA damage Checkpoint 1 and repressing MIR22HG/miR-22-3p.Molecular cancer · 2022Article
- Review
- Ap4 is rate limiting for intestinal tumor formation by controlling the homeostasis of intestinal stem cells.Nature communications · 2018Article
- Differential cellular responses by oncogenic levels of c-Myc expression in long-term confluent retinal pigment epithelial cells.Molecular and cellular biochemistry · 2018Article
- Evaluating the prognostic value and functional roles of transcription factor AP4 in colorectal cancer.Oncology letters · 2018Article
- Transcription factor AP-4 promotes tumorigenic capability and activates the Wnt/β-catenin pathway in hepatocellular carcinoma.Theranostics · 2018Article
- Integrative microRNA and mRNA deep-sequencing expression profiling in endemic Burkitt lymphoma.BMC cancer · 2017Article
- Chemical-agnostic hazard prediction: statistical inference ofComputational toxicology (Amsterdam, Netherlands) · 2017Article
- Regulation of activating protein-4-associated metastases of non-small cell lung cancer cells by miR-144.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- ChIP-on-chip analysis of thyroid hormone-regulated genes and their physiological significance.Oncotarget · 2016Article
- The Quest for Targets Executing MYC-Dependent Cell Transformation.Frontiers in oncology · 2016Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AP4 represents a c-MYC-inducible bHLH-LZ transcription factor, which displays elevated expression in many types of tumors. We found that serum-starved AP4-deficient mouse embryo fibroblasts (MEFs) were unable to resume proliferation and showed a delayed S-phase entry after restimulation. Furthermore, they accumulated as tetraploid cells due to a cytokinesis defect. In addition, AP4 was required for c-MYC-induced cell cycle re-entry. AP4-deficient MEFs displayed decreased expression of CDK2 (cyclin-dependent kinase 2), which we characterized as a conserved and direct AP4 target. Activation of an AP4 estrogen receptor fusion protein (AP4-ER) enhanced proliferation of human diploid fibroblasts in a CDK2-dependent manner. However, in contrast to c-MYC-ER, AP4-ER activation was not sufficient to induce cell cycle re-entry or apoptosis in serum-starved MEFs. AP4-deficiency was accompanied by increased spontaneous and c-MYC-induced DNA damage in MEFs. Furthermore, c-MYC-induced apoptosis was decreased in AP4-deficient MEFs, suggesting that induction of apoptosis by c-MYC is linked to its ability to activate AP4 and thereby cell cycle progression. Taken together, these results indicate that AP4 is a central mediator and coordinator of cell cycle progression in response to mitogenic signals and c-MYC activation. Therefore, inhibition of AP4 function may represent a therapeutic approach to block tumor cell proliferation.
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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.