ArticleOncotarget2018
c-Myb and C/EBPβ regulate OPN and other senescence-associated secretory phenotype factors.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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
19 citing papers in PubMed, 25 citations in OpenAlex.
- Cellular Senescence Triggered by Food and Environmental Genotoxins.International journal of molecular sciences · 2026Review
- Natural Products as Anti-Senescence-Associated Secretory Phenotype (SASP) Agents.Current medicinal chemistry · 2026Review
- The mitochondrial logic of inflammaging: how energy imbalance drives fibroblast SASP and tissue-specific aging.Frontiers in immunology · 2026Review
- Integrating Senescence and Oxidative Stress in Cardiac Disease.International journal of molecular sciences · 2025Review
- The states of senescent cells.Biochemical Society transactions · 2025Review
- Profiles of Monocyte Subsets and Fibrosis-Related Genes in Patients with Muscular Dystrophy Undergoing Intermittent Prednisone Therapy.International journal of molecular sciences · 2025Article
- Molecular Regulation of SASP in Cellular Senescence: Therapeutic Implications and Translational Challenges.Cells · 2025Review
- From modulation of cellular plasticity to potentiation of therapeutic resistance: new and emerging roles of MYB transcription factors in human malignancies.Cancer metastasis reviews · 2024Review
- Review
- Targeting epiregulin in the treatment-damaged tumor microenvironment restrains therapeutic resistance.Oncogene · 2022Article
- Cellular senescence: the good, the bad and the unknown.Nature reviews. Nephrology · 2022Review
- Cellular senescence and the tumour microenvironment.Molecular oncology · 2022Review
- Histone H2A ubiquitination resulting from Brap loss of function connects multiple aging hallmarks and accelerates neurodegeneration.iScience · 2022Article
- Article
- Liver osteopontin is required to prevent the progression of age-related nonalcoholic fatty liver disease.Aging cell · 2020Article
- Dominant-Negative ATF5 Compromises Cancer Cell Survival by Targeting CEBPB and CEBPD.Molecular cancer research : MCR · 2020Article
- Cellular Senescence in Kidney Fibrosis: Pathologic Significance and Therapeutic Strategies.Frontiers in pharmacology · 2020Review
- Unmasking senescence: context-dependent effects of SASP in cancer.Nature reviews. Cancer · 2019Review
- Targeting SPINK1 in the damaged tumour microenvironment alleviates therapeutic resistance.Nature communications · 2018Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Tumorigenesis results from the convergence of cell autonomous mutations and corresponding stromal changes that promote tumor cell growth. Senescent cells, which secrete a plethora of pro-tumorigenic factors termed the senescence-associated secretory phenotype (SASP), play an important role in tumor formation. Investigation into SASP regulation revealed that many but not all SASP factors are subject to NF-kB and p38MAPK regulation. However, many pro-tumorigenic SASP factors, including osteopontin (OPN), are not responsive to these canonical pathways leaving the regulation of these factors an open question. We report that the transcription factor c-Myb regulates OPN, IL-6, and IL-8 in addition to 57 other SASP factors. The regulation of OPN is direct as c-Myb binds to the OPN promoter in response to senescence. Further, OPN is also regulated by the known SASP regulator C/EBPβ. In response to senescence, the full-length activating C/EBPβ isoform LAP2 increases binding to the OPN, IL-6, and IL-8 promoters. The importance of both c-Myb and C/EBPβ is underscored by our finding that the depletion of either factor reduces the ability of senescent fibroblasts to promote the growth of preneoplastic epithelial 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.