ArticleThe Journal of clinical investigation2016
E2f8 mediates tumor suppression in postnatal liver development.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.
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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
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.
- Carcinogenesis effects of E2F transcription factor 8 (E2F8) in hepatocellular carcinoma outcomes: an integrated bioinformatic report.Bioscience reports · 2020Pooled it
- An epithelial cell fate-driven predictive model for liver metastasis risk in primary colorectal cancer through single-cell and multi-omics integration.Journal of translational medicine · 2026Article
- Mechanisms driving resistance to oxidative stress during endometrial stromal cell decidualization†.Biology of reproduction · 2026Review
- Chronobiology of neurotropic viruses: rhythmic viral entry and arrhythmic host clocks.Cell discovery · 2026Article
- Diploid hepatocytes resist acetaminophen-induced liver injury through suppressed JNK signaling.Cell death & disease · 2026Article
- Vacuolar Protein Sorting 35 Controls Hepatocellular Proliferation Through SRC Signaling and Promotes Diethyl Nitrosamine-Induced Tumor Initiation.Cellular and molecular gastroenterology and hepatology · 2026Article
- Identification of an E2Fs-based gene signature for predicting prognosis and therapeutic response in colorectal cancer.Discover oncology · 2025Article
- Integrative analysis identifies the atypical repressor E2F8 as a targetable transcriptional activator driving lethal prostate cancer.Oncogene · 2025Article
- Small molecule-mediated inhibition of the oxidoreductase ERO1A restrains aggressive breast cancer by impairing VEGF and PD-L1 in the tumor microenvironment.Cell death & disease · 2025Article
- The E2F family: a ray of dawn in cardiomyopathy.Molecular and cellular biochemistry · 2025Review
- Identification of the role of MED6 in the development and prognosis of lung adenocarcinoma based on multi-omics profiling.Journal of Cancer · 2025Article
- Insight into mammary gland development and tumor progression in an E2F5 conditional knockout mouse model.Oncogene · 2024Article
- Manzamine A reduces androgen receptor transcription and synthesis by blocking E2F8-DNA interactions and effectively inhibits prostate tumor growth in mice.Molecular oncology · 2024Article
- Article
- The Ploidy State as a Determinant of Hepatocyte Proliferation.Seminars in liver disease · 2023Review
- Article
- Cellular polyploidy in organ homeostasis and regeneration.Protein & cell · 2023Article
- Significance of RB Loss in Unlocking Phenotypic Plasticity in Advanced Cancers.Molecular cancer research : MCR · 2023Article
- Review
- Transcription factor E2F8 is a therapeutic target in the basal-like subtype of breast cancer.Frontiers in oncology · 2023Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
33 authors at 5 institutions in 2 countries.
Funding
Abstract
E2F-mediated transcriptional repression of cell cycle-dependent gene expression is critical for the control of cellular proliferation, survival, and development. E2F signaling also interacts with transcriptional programs that are downstream of genetic predictors for cancer development, including hepatocellular carcinoma (HCC). Here, we evaluated the function of the atypical repressor genes E2f7 and E2f8 in adult liver physiology. Using several loss-of-function alleles in mice, we determined that combined deletion of E2f7 and E2f8 in hepatocytes leads to HCC. Temporal-specific ablation strategies revealed that E2f8's tumor suppressor role is critical during the first 2 weeks of life, which correspond to a highly proliferative stage of postnatal liver development. Disruption of E2F8's DNA binding activity phenocopied the effects of an E2f8 null allele and led to HCC. Finally, a profile of chromatin occupancy and gene expression in young and tumor-bearing mice identified a set of shared targets for E2F7 and E2F8 whose increased expression during early postnatal liver development is associated with HCC progression in mice. Increased expression of E2F8-specific target genes was also observed in human liver biopsies from HCC patients compared to healthy patients. In summary, these studies suggest that E2F8-mediated transcriptional repression is a critical tumor suppressor mechanism during postnatal liver development.
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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.