Affinage

E2F8

Transcription factor E2F8 · UniProt A0AVK6

Length
867 aa
Mass
94.2 kDa
Annotated
2026-06-09
66 papers in source corpus 40 papers cited in narrative 40 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

E2F8 is an atypical E2F-family transcription factor that controls cell proliferation, embryonic development, and the DNA-damage response through a non-canonical mode of DNA binding (PMID:15722552, PMID:16179649, PMID:15897886, PMID:18194653). Unlike canonical E2Fs, it contains two tandem DNA-binding domains—both required for DNA occupancy—and binds DNA independently of DP partners and retinoblastoma protein, lacking the dimerization and activation domains those proteins require (PMID:15722552, PMID:16179649, PMID:15897886). It homodimerizes and forms heterodimers with the related E2F7, and the two together occupy target promoters as a repressive DNA-binding complex; concurrent loss of E2f7 and E2f8 (but neither alone) causes massive apoptosis and embryonic lethality that is rescued by removal of E2f1 or p53, placing the E2F7/E2F8 complex upstream of the E2F1–p53 axis (PMID:15722552, PMID:16179649, PMID:18194653). As a repressor, E2F8 is induced by DNA damage to silence the E2F1 promoter and enforce cell-cycle arrest, antagonizes the proliferation-promoting activities of activator E2Fs by co-occupying shared promoters with opposing effect, and drives hepatocyte and decidual polyploidization by suppressing cytokinesis genes such as CDK1 (PMID:18202719, PMID:23064264, PMID:25892397). In the liver this repressive program constitutes a tumor-suppressor function whose loss—or disruption of the DNA-binding domain—causes hepatocellular carcinoma (PMID:27454291). E2F8 protein abundance oscillates across the cell cycle: Cdk1 phosphorylation of N-terminal threonines adjacent to APC/C recognition motifs licenses APC/C^Cdh1-dependent degradation at mitotic exit, PP2A dephosphorylation couples its accumulation to G1, and Cyclin F provides additional G2 control (PMID:31995441). Beyond repression, E2F8 acts context-dependently as a transcriptional activator: with HIF1 it directly activates VEGFA to drive angiogenesis (PMID:22903062), and across diverse cancers it directly binds and activates cell-cycle, replication, and DNA-repair genes including CCND1, CCNE1/2, RRM2, UHRF1, MASTL, and RAD51 to promote proliferation, DNA repair, and chemoresistance (PMID:20068156, PMID:26089541, PMID:26992224, PMID:37863324, PMID:38095232). In AR-negative castration-resistant prostate cancer this activator role dominates, with E2F8 driving an oncogenic cistrome (PMID:39613933).

Mechanistic history

Synthesis pass · year-by-year structured walk · 8 steps
  1. 2005 High

    Established that E2F8 is a structurally distinct E2F that binds DNA and represses transcription without the dimerization and Rb-binding machinery of canonical family members, defining it as an atypical repressor.

    Evidence Sequence analysis, recombinant DNA-binding assays, promoter reporters, and overexpression in primary MEFs; domain mutagenesis showing both DNA-binding domains are required

    PMID:15722552 PMID:15897886 PMID:16179649

    Open questions at the time
    • Endogenous target gene set not yet defined
    • Physiological partners beyond homodimer not yet identified
  2. 2008 High

    Resolved how E2F8 acts in vivo by showing it functions as an E2F7/E2F8 repressor complex that restrains the E2F1–p53 apoptotic axis, explaining its essential role in development.

    Evidence E2f7/E2f8 single and double knockout mice, ChIP on the E2f1 promoter, and genetic epistasis with E2f1 and p53 loss-of-function

    PMID:18194653 PMID:18202719

    Open questions at the time
    • Determinants of homo- versus hetero-dimer choice unknown
    • How DNA damage induces E2F7/8 not mechanistically resolved
  3. 2012 High

    Connected E2F8 repression to physiological ploidy control and to context-dependent activation, showing it suppresses cytokinesis genes to drive hepatocyte polyploidization yet co-activates VEGFA with HIF1.

    Evidence Liver-specific E2f8 knockout with E2f1 epistasis and promoter ChIP; VEGFA reporter, ChIP, and zebrafish/mouse double knockouts with vascular phenotypes

    PMID:22903062 PMID:23064264

    Open questions at the time
    • Molecular switch between repressive and activating modes unresolved
    • How HIF1 redirects E2F8 to non-canonical elements unclear
  4. 2016 High

    Demonstrated that E2F8's DNA-binding activity is the basis of a bona fide tumor-suppressor function with a defined developmental window, by knock-in phenocopy of the null allele.

    Evidence Temporal conditional knockouts, DNA-binding-domain mutant knock-in, and ChIP-seq in postnatal liver

    PMID:27454291

    Open questions at the time
    • Why the tumor-suppressor window is restricted to early postnatal life is unexplained
    • Genome-wide target overlap with E2F7 in liver not fully mapped
  5. 2020 High

    Defined how E2F8 protein levels are timed across the cell cycle, identifying a Cdk1/PP2A phospho-switch that gates APC/C^Cdh1-dependent degradation, with Cyclin F adding G2 control.

    Evidence Human cell-free systems reconstituting inter-mitotic and G1 phases with kinase/phosphatase perturbations and APC/C degradation assays

    PMID:31995441

    Open questions at the time
    • In vivo physiological consequence of mis-timed degradation untested
    • Precise degron and phospho-site mapping deferred to later work
  6. 2023 High

    Broadened the activator role of E2F8 by showing direct activation of replication/repair effectors that drive proliferation and chemoresistance across multiple cancers.

    Evidence ChIP-qPCR, reporter and DNA-pulldown assays plus knockdown/xenograft for RRM2, RAD51, CENPL, and others

    PMID:37863324 PMID:38095232 PMID:38522807

    Open questions at the time
    • Cofactors that convert E2F8 to an activator in cancer not identified
    • Whether activation requires displacement of the E2F7/8 repressor complex unknown
  7. 2024 High

    Showed that in AR-negative castration-resistant prostate cancer E2F8 operates predominantly as a transcriptional activator of an oncogenic cistrome, establishing a lineage-specific reversal of its canonical repressor identity.

    Evidence E2F8 ChIP-seq and RNA-seq integration with CRISPR/CasRx knockdown and xenograft growth readouts

    PMID:39613933

    Open questions at the time
    • Chromatin context driving activation versus repression not defined
    • Generality across other AR-negative tumors untested
  8. 2025 High

    Refined the degradation model by mapping APC/C recognition motifs and Cdk1-phosphorylated threonines in flexible N-terminal domains, showing PP2A acts as the molecular switch coupling E2F8/E2F7 turnover to G1 and the rise of E2F1.

    Evidence Cell-free reconstitution across mitotic-to-G1 transitions with Cdk1/PP2A perturbations and degron mutagenesis (preprint)

    PMID:bio_10.1101_2025.02.23.639703

    Open questions at the time
    • Preprint not yet peer-reviewed
    • Structural basis of APC/C engagement not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • The molecular determinant that toggles E2F8 between an E2F7-partnered repressor and a context-dependent transcriptional activator remains unresolved.
  • No defined cofactor or modification that switches repression to activation
  • Relationship between activator cistromes and the canonical E2F7/8 repressive complex unmapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 5 GO:0003677 DNA binding 3
Localization
GO:0005634 nucleus 2
Pathway
R-HSA-1640170 Cell Cycle 4 R-HSA-73894 DNA Repair 3 R-HSA-74160 Gene expression (Transcription) 3
Partners
E2F7HIF1KNTC1PAFAH1B3
Complex memberships
E2F7/E2F8 repressor complex

Evidence

Reading pass · 40 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2005 E2F8 contains two distinct DNA-binding domains (unlike canonical E2Fs), binds DNA without DP co-factors, lacks DP-dimerization/retinoblastoma-binding/transcriptional activation domains, and functions as a transcriptional repressor that inhibits E2F-driven promoters and slows cell proliferation when overexpressed in primary MEFs. Sequence analysis, recombinant protein DNA-binding assay, promoter reporter assays, overexpression in primary mouse embryonic fibroblasts The Journal of biological chemistry / Nucleic acids research / Oncogene High 15722552 15897886 16179649
2005 The integrity of both DNA-binding domains of E2F8 is required for DNA binding; mutations disrupting either domain abolish DNA binding activity. Active-site/domain mutagenesis, DNA-binding assay Oncogene Medium 15897886
2005 E2F8 can homodimerize and is expressed in the same adult tissues as E2F7, suggesting overlapping roles; E2F8 overexpression significantly slows proliferation of primary MEFs. Co-immunoprecipitation (homodimerization), overexpression proliferation assay The Journal of biological chemistry Medium 15722552 16179649
2008 E2F7 and E2F8 form homo- and heterodimers that occupy target gene promoters (including E2f1) and act as transcriptional repressors; combined loss of E2f7 and E2f8 (but not either alone) causes massive apoptosis and embryonic lethality. Genetic suppression by loss of E2f1 or p53 rescues apoptosis, placing E2F7/E2F8 upstream of the E2F1–p53 apoptotic axis. Mouse knockout genetics (E2f7 and E2f8 single and double knockouts), chromatin immunoprecipitation (ChIP) on target promoters, epistasis (E2f1 and p53 loss-of-function rescue) Developmental cell High 18194653
2008 E2F7 and E2F8 are induced by DNA-damaging agents, bind the E2F1 promoter as a DNA-binding complex, repress E2F1 expression, and are required for cell-cycle effects of the DNA-damage response; depletion of either subunit increases E2F1 expression and prevents DNA-damage-induced cell-cycle arrest. ChIP on E2F1 and other E2F-responsive gene promoters, siRNA knockdown with cell-cycle and E2F1 expression readouts EMBO reports High 18202719
2007 In a yeast expression system, E2F8 activates heterotrimeric G proteins as a guanine nucleotide exchange factor (GEF) for Gαi; epistasis showed E2F8 acts at the level of G proteins (not receptors), is antagonized by the GTPase-activating protein RGS4, and the first 200 N-terminal residues carry most activity. Yeast expression cloning, epistasis with Gα subunits and RGS4, receptor-independent activation assay Journal of molecular signaling Low 17394670
2012 E2F8 is required for hepatocyte binucleation and polyploidization in mice; E2f8 deficiency leads to increased expression of E2F target genes that promote cytokinesis, preventing polyploidization. E2F8 and E2F1 occupy the same subset of target promoters with opposing effects (E2F8 represses, E2F1 activates); loss of E2f1 enhances polyploidization and suppresses the E2f8-deficiency polyploidization defect. Mouse liver-specific knockout (E2f8 and E2f1 loss-of-function), ChIP on target promoters, epistasis Nature cell biology High 23064264
2012 E2F7 and E2F8 directly bind and transcriptionally activate the VEGFA promoter in a HIF1-dependent complex, independent of canonical E2F binding elements, thereby promoting angiogenesis; simultaneous deletion of E2F7/8 in zebrafish and mice causes severe vascular defects. VEGFA promoter reporter assay, ChIP, zebrafish and mouse double knockout with vascular phenotype readout The EMBO journal High 22903062
2010 E2F8 binds regulatory elements of the cyclin D1 (CCND1) promoter and activates its transcription, promoting S-phase accumulation in hepatocellular carcinoma cells. ChIP, promoter reporter assay, overexpression and knockdown with cell-cycle and gene expression readouts Cancer research Medium 20068156
2014 Rb and E2F8 co-suppress E2F target genes critical for DNA replication during erythroid terminal differentiation; loss of both Rb and E2f8 synergizes to increase E2F2 binding to target promoters and causes stressed DNA replication, DNA damage, and defective erythropoiesis rescued by inactivation of E2f2. Erythroid-specific Rb and E2f8 conditional knockouts, gene expression profiling, ChIP, epistasis with E2f2 Molecular and cellular biology High 24865965
2015 E2F8 directly binds the UHRF1 promoter and activates its transcription in lung cancer cells, as determined by ChIP and promoter activity assays; E2F8 depletion reduces UHRF1 expression and inhibits tumor growth. ChIP, promoter reporter assay, siRNA knockdown, xenograft tumor growth Journal of the National Cancer Institute Medium 26089541
2015 E2F8 is highly expressed in decidual cells in mice, is regulated by progesterone through the HB-EGF/EGFR/ERK/STAT3 signaling pathway, and transcriptionally suppresses CDK1, thereby triggering polyploidization of decidual cells. In vivo mouse decidualization model, signaling pathway inhibitor studies, ChIP/gene expression analysis of CDK1 Cell cycle Medium 25892397
2015 E2F8 promotes FABP3 expression in liver during diet-induced obesity in zebrafish; E2f8 morpholino knockdown suppresses fabp3 expression and ameliorates hepatic steatosis, and E2F8 overexpression in human HepG2 cells promotes FABP3 expression. Morpholino knockdown in zebrafish, overexpression in human HepG2 cells, transcriptome/proteome analysis Nutrition & metabolism Medium 26052340
2016 E2F8's DNA-binding activity is essential for its tumor suppressor function in postnatal liver; disruption of E2F8 DNA-binding domain phenocopies E2f8 null allele and leads to HCC. Combined hepatocyte-specific deletion of E2f7 and E2f8 causes HCC, with E2F8's critical tumor suppressor window during the first 2 weeks of postnatal life. Conditional knockout mice (temporal-specific ablation), DNA-binding domain mutant knock-in, chromatin occupancy profiling (ChIP-seq), gene expression profiling The Journal of clinical investigation High 27454291
2016 E2F8 directly binds the CCNE1 and CCNE2 promoters and transcriptionally upregulates their expression, accelerating G1-to-S phase transition in breast cancer cells. ChIP, promoter reporter assay, overexpression and knockdown with cell-cycle readout Oncotarget Medium 26992224
2017 E2F8 directly binds the MASTL promoter (validated by dual luciferase assay and ChIP-qPCR) and transcriptionally activates MASTL; E2F8 overexpression alleviates cisplatin-induced G2/M arrest by promoting MASTL-mediated mitotic entry, an effect cancelled by MASTL inhibition. Dual luciferase assay, ChIP-qPCR, overexpression/inhibition experiments with cell-cycle readout Biomedicine & pharmacotherapy Medium 28605876
2019 RNA-binding protein NONO post-transcriptionally regulates E2F8 expression by binding to E2F8 mRNA, as shown by RNA immunoprecipitation-sequencing (RIP-seq); NONO knockdown reduces E2F8 protein levels and suppresses breast cancer cell proliferation. RIP-sequencing, expression microarray integration, siRNA knockdown of NONO Cancer science Medium 31733123
2020 E2F8 protein degradation is controlled throughout the cell cycle by an interlocking dephosphorylation switch: Cdk1 phosphorylation promotes APC/CCdh1-dependent degradation at mitotic exit; PP2A dephosphorylation coupled to the G1 phase allows E2F8 accumulation; Cyclin F regulates E2F8 specifically in G2 phase. Human cell-free systems reconstituting inter-mitotic and G1 phases, APC/C degradation assays, phosphorylation analysis Molecular biology of the cell High 31995441
2019 E2F8 is a transcriptional regulator of gluconeogenesis in primary mouse hepatocytes; adenovirus-mediated E2F8 overexpression upregulates PGC-1α, PEPCK, and G6Pase expression and increases glucose output, while E2F8 knockdown increases insulin sensitivity. Adenovirus-mediated overexpression, siRNA knockdown, glucose output assays, gene expression analysis in primary mouse hepatocytes and diabetic mouse models Biochemistry. Biokhimiia Medium 31870257
2020 E2F8 knockdown in pancreatic beta cells (MIN6) reduces Abcc8 (KATP channel subunit) expression by ~30%, impairing ATP-sensitive K+ channel-dependent insulin secretion. siRNA knockdown in MIN6 cells, gene expression analysis, insulin secretion assay Diabetologia Medium 32356104
2022 E2F8 functions as a transcriptional repressor of Il9 in CD4+ T cells; TGF-β and IL-4 signaling induces pSmad3L-Ser213 via p38, which is necessary for Il9 transcription, and E2F8 represses this Il9 transcription. siRNA-mediated knockdown of E2f8 promotes tumor growth in mouse tumor models, while knockdown of Dbp (activator) suppresses it. siRNA knockdown in Th9 differentiation, mouse tumor models, Smad3 phosphorylation analysis, Il9 promoter studies Nature communications Medium 36241625
2023 E2F8 directly binds the RRM2 promoter and transcriptionally activates RRM2 expression in lung adenocarcinoma cells; E2F8-driven RRM2 upregulation promotes DNA synthesis and cell cycle progression; E2F8 knockdown combined with WEE1 inhibitor MK-1775 synergistically suppresses tumor growth. Reporter gene assay, ChIP-qPCR, DNA pulldown-Western blot, overexpression/knockdown, in vitro and in vivo xenograft experiments Biochemical pharmacology High 37863324
2023 E2F8 directly binds the NUSAP1 promoter and activates its transcription (confirmed by ChIP and dual-luciferase assay); E2F8-mediated NUSAP1 upregulation inhibits cisplatin-induced DNA damage and enhances cisplatin resistance in HCC cells. ChIP, dual-luciferase reporter assay, overexpression/knockdown, comet assay, flow cytometry International journal of toxicology Medium 37331996
2024 E2F8 directly binds the CENPL promoter and transcriptionally activates CENPL expression; E2F8-CENPL axis promotes homologous recombination DNA repair and confers chemoresistance; CENPL overexpression partially rescues DNA damage repair defects caused by E2F8 knockdown. ChIP, reporter assay, knockdown/overexpression, HR repair assay, drug sensitivity assay Cellular signalling Medium 38522807
2024 IGF-I activates the PI3K/AKT pathway to upregulate E2F8, which transcriptionally activates RAD51 expression to promote homologous recombination repair and protect granulosa cells from hypoxia-induced apoptosis. PI3K/AKT pathway inhibition, E2F8 knockdown/overexpression, RAD51 promoter analysis, HR repair assay, apoptosis assay in porcine granulosa cells FASEB journal Medium 38095232
2024 E2F8 directly binds the PDK1 promoter (validated by dual-luciferase and ChIP) and transcriptionally activates PDK1; E2F8/PDK1 axis mediates DNA damage repair to promote cisplatin resistance in lung adenocarcinoma. Dual-luciferase assay, ChIP, overexpression/knockdown, DNA damage assay (comet, γ-H2AX), NHEJ reporter, xenograft Pharmacology Medium 38810606
2024 E2F8 transcriptionally activates ENO1 expression (confirmed by ChIP and RNA-seq) and promotes trophoblast invasion by inhibiting SFRP1/4 to activate Wnt signaling. ChIP, plasmid transfection, RNA-seq, western blotting, transwell invasion assay, immunofluorescence FASEB journal Medium 38661062
2024 E2F8 directly activates androgen receptor (AR) transcription; the marine compound manzamine A blocks E2F8-DNA interactions, suppressing E2F8-dependent AR and AR-V7 synthesis in prostate cancer cells and reducing tumor growth in xenograft models. RNA-seq, protein modeling of E2F8-DNA interaction, cell line and xenograft experiments with manzamine A, AR expression analysis Molecular oncology Medium 38605607
2024 KNTC1 physically binds E2F8 protein and facilitates its nuclear translocation, enhancing E2F8-mediated transcriptional activation of MYC; MYC in turn transcriptionally upregulates KNTC1, forming a positive feedback loop driving PI3K/AKT/mTOR activation in bladder cancer. Co-immunoprecipitation, ChIP, luciferase reporter assay, nuclear fractionation, gene knockdown/overexpression, xenograft Journal of experimental & clinical cancer research Medium 41639725
2024 E2F8 promotes TJP1 transcription (Halo-E2F8 overexpression increases TJP1 expression and transcription); TJP1 suppresses extravillous trophoblast invasion. Loss of E2F8 increases trophoblast invasiveness through reduced TJP1 and increased MMP-1 production. E2F8 overexpression (Halo-tagged), E2F8 shRNA knockdown, TJP1 knockdown/overexpression, invasion assay, MMP-1 measurement Molecular and cellular endocrinology Medium 38795825
2024 E2F8 transcriptionally activates TPX2 expression; E2F8-TPX2 axis promotes glycolysis and angiogenesis, cancer progression, and reduces cisplatin and apatinib sensitivity in liver cancer cells. Bioinformatics plus qRT-PCR, CCK-8, Transwell, flow cytometry, angiogenesis assay, E2F8 overexpression reversing TPX2 knockdown effects Cytotechnology Low 39435417
2024 E2F8 directly binds the MCM7 promoter and activates MCM7 transcription (confirmed by ChIP); MCM7 overexpression rescues the suppressive effects of E2F8 knockdown on bladder cancer cell malignant phenotypes. ChIP on MCM7 promoter, overexpression rescue experiment, knockdown with proliferation/invasion assays Biochemistry and cell biology Medium 39601318
2025 E2F8 is a direct APC/C substrate; flexible N-terminal domains contain APC/C recognition motifs adjacent to critical Thr residues whose phosphorylation by Cdk1 is rate-limiting for degradation; PP2A dephosphorylation of these residues acts as a molecular switch coupling E2F8 and E2F7 degradation to the G1 phase, coinciding with the rise of E2F1. Cell-free systems (inter-mitotic, G1, and prometaphase-to-G1 transitions), Cdk1 and PP2A activity perturbations, APC/C degradation assays, domain mutagenesis bioRxiv (preprint)preprint High bio_10.1101_2025.02.23.639703
2025 E2F8 transcriptionally activates SPC25 expression (confirmed by dual-luciferase and ChIP); E2F8/SPC25 axis promotes glutamine metabolism to facilitate immune escape in lung adenocarcinoma; SPC25 overexpression rescues immune escape suppression caused by E2F8 knockdown. Dual-luciferase assay, ChIP, E2F8/SPC25 knockdown/overexpression, co-culture immune assay, glutamine metabolism measurements Immunology Medium 39829079
2025 E2F8 transcriptionally activates GRPEL2 expression (confirmed by luciferase reporter and ChIP assays); E2F8/GRPEL2 axis promotes colorectal cancer progression through mitochondrial dysregulation; TIGAR interacts with GRPEL2 protein (co-IP) as a downstream effector. Luciferase reporter, ChIP, Co-IP (GRPEL2-TIGAR interaction), knockdown/overexpression, in vivo metastasis model Journal of translational medicine Medium 40269881
2025 E2F8 transcriptionally activates DTL expression by binding its promoter; E2F8/DTL axis activates the MAPK signaling pathway in endometrial cancer; DTL knockdown enhances PDCD4 ubiquitination; DTL overexpression or PDCD4 knockdown rescues the growth-suppressive effects of E2F8 knockdown. ChIP, bioinformatics, functional assays (proliferation, migration, invasion), xenograft, ubiquitination assay Reproductive sciences Medium 41461624
2025 E2F8 transcriptionally activates EGFL6 by binding its promoter (confirmed by dual luciferase assay); EGFL6 overexpression rescues proliferation, migration, and invasion suppressed by E2F8 knockdown in endometrial cancer cells. Dual luciferase assay, shRNA knockdown, overexpression rescue, CCK-8 and Transwell assays, xenograft Biology of the cell Medium 41555699
2025 E2F8 coordinates with PAFAH1B3 to promote VEGFA transcription in gastric cancer cells; VEGFA overexpression rescues defects caused by PAFAH1B3 knockdown; in vivo xenograft experiments confirm VEGFA as a downstream effector of this pathway. Transcriptomic profiling, VEGFA overexpression rescue, xenograft, PAFAH1B3 knockdown Biochemical pharmacology Low 42140448
2025 E2F8 transcriptionally activates RRM2 expression in gallbladder cancer; E2F8-RRM2 axis drives gemcitabine resistance; a small-molecule HIT-4 identified by virtual screening disrupts E2F8-DNA interaction, reduces RRM2 expression, and synergizes with PARP inhibitors to suppress tumor growth in vivo and in patient-derived organoids. CRISPR-Cas9 genome-wide knockout screen, ChIP (implied by context of E2F8-RRM2 transcriptional regulation), virtual screening, cell viability/apoptosis assays, xenograft, patient-derived organoids Journal of experimental & clinical cancer research Medium 41392282
2024 In AR-negative castration-resistant prostate cancer, E2F8 non-canonically activates (rather than represses) target oncogenes; CRISPR/CasRx-mediated knockdown of E2F8 downregulates target oncogenes and inhibits AR-negative CRPC growth in vitro and in xenograft models. E2F8 cistrome profiling (ChIP-seq), transcriptome profiling (RNA-seq), CRISPR/CasRx knockdown, xenograft model Oncogene High 39613933

Source papers

Stage 0 corpus · 66 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 Synergistic function of E2F7 and E2F8 is essential for cell survival and embryonic development. Developmental cell 182 18194653
2005 Cloning and characterization of mouse E2F8, a novel mammalian E2F family member capable of blocking cellular proliferation. The Journal of biological chemistry 158 15722552
2005 Characterization of E2F8, a novel E2F-like cell-cycle regulated repressor of E2F-activated transcription. Nucleic acids research 145 16179649
2012 E2F8 is essential for polyploidization in mammalian cells. Nature cell biology 138 23064264
2008 DNA-damage response control of E2F7 and E2F8. EMBO reports 111 18202719
2012 E2F7 and E2F8 promote angiogenesis through transcriptional activation of VEGFA in cooperation with HIF1. The EMBO journal 107 22903062
2005 E2F-8: an E2F family member with a similar organization of DNA-binding domains to E2F-7. Oncogene 101 15897886
2010 E2F8 contributes to human hepatocellular carcinoma via regulating cell proliferation. Cancer research 91 20068156
2018 Upregulated miR-1258 regulates cell cycle and inhibits cell proliferation by directly targeting E2F8 in CRC. Cell proliferation 90 30144184
2015 E2F8 as a Novel Therapeutic Target for Lung Cancer. Journal of the National Cancer Institute 88 26089541
2016 E2f8 mediates tumor suppression in postnatal liver development. The Journal of clinical investigation 81 27454291
2019 RNA-binding protein NONO promotes breast cancer proliferation by post-transcriptional regulation of SKP2 and E2F8. Cancer science 75 31733123
2017 E2F8, a direct target of miR-144, promotes papillary thyroid cancer progression via regulating cell cycle. Journal of experimental & clinical cancer research : CR 59 28270228
2016 Synergistic functions of E2F7 and E2F8 are critical to suppress stress-induced skin cancer. Oncogene 56 27452520
2016 Upregulation of E2F8 promotes cell proliferation and tumorigenicity in breast cancer by modulating G1/S phase transition. Oncotarget 53 26992224
2018 HOXD-AS1/miR-130a sponge regulates glioma development by targeting E2F8. International journal of cancer 52 29341117
2015 Involvement of atypical transcription factor E2F8 in the polyploidization during mouse and human decidualization. Cell cycle (Georgetown, Tex.) 50 25892397
2016 Geraniol suppresses prostate cancer growth through down-regulation of E2F8. Cancer medicine 48 27683099
2015 E2F8 promotes hepatic steatosis through FABP3 expression in diet-induced obesity in zebrafish. Nutrition & metabolism 45 26052340
2008 E2F7 and E2F8 keep the E2F family in balance. Developmental cell 39 18194644
2017 E2F8 is a Potential Therapeutic Target for Hepatocellular Carcinoma. Journal of Cancer 38 28607595
2018 miR-223-5p Suppresses Tumor Growth and Metastasis in Non-Small Cell Lung Cancer by Targeting E2F8. Oncology research 35 29615147
2017 Metformin induces cell cycle arrest at the G1 phase through E2F8 suppression in lung cancer cells. Oncotarget 33 29254182
2020 E2F8 regulates the proliferation and invasion through epithelial-mesenchymal transition in cervical cancer. International journal of biological sciences 28 31929759
2020 Long noncoding RNA SNHG6 promotes proliferation and angiogenesis of cholangiocarcinoma cells through sponging miR-101-3p and activation of E2F8. Journal of Cancer 26 32226515
2017 E2F8 confers cisplatin resistance to ER+ breast cancer cells via transcriptionally activating MASTL. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 26 28605876
2020 E2F8 Induces Cell Proliferation and Invasion through the Epithelial-Mesenchymal Transition and Notch Signaling Pathways in Ovarian Cancer. International journal of molecular sciences 21 32823614
2023 Emerging role of E2F8 in human cancer. Biochimica et biophysica acta. Molecular basis of disease 20 37164180
2020 Cell cycle oscillators underlying orderly proteolysis of E2F8. Molecular biology of the cell 19 31995441
2022 Opposing functions of circadian protein DBP and atypical E2F family E2F8 in anti-tumor Th9 cell differentiation. Nature communications 17 36241625
2019 Knockdown of E2F8 Suppresses Cell Proliferation in Colon Cancer Cells by Modulating the NF-κB Pathway. Annals of clinical and laboratory science 16 31471336
2020 E2f8 and Dlg2 genes have independent effects on impaired insulin secretion associated with hyperglycaemia. Diabetologia 14 32356104
2019 Hsa_circ_0002468 Regulates the Neuronal Differentiation of SH-SY5Y Cells by Modulating the MiR-561/E2F8 Axis. Medical science monitor : international medical journal of experimental and clinical research 14 30951518
2023 E2F8 exerts cancer-promoting effects by transcriptionally activating RRM2 and E2F8 knockdown synergizes with WEE1 inhibition in suppressing lung adenocarcinoma. Biochemical pharmacology 12 37863324
2018 The role of E2F8 in the human placenta. Molecular medicine reports 12 30387815
2014 Inactivation of Rb and E2f8 synergizes to trigger stressed DNA replication during erythroid terminal differentiation. Molecular and cellular biology 11 24865965
2023 Transcription Factor E2F8 Promotes Cisplatin Resistance in Hepatocellular Carcinoma by Regulating DNA Damage via NUSAP1. International journal of toxicology 10 37331996
2020 Carcinogenesis effects of E2F transcription factor 8 (E2F8) in hepatocellular carcinoma outcomes: an integrated bioinformatic report. Bioscience reports 9 31990034
2024 E2F8-CENPL pathway contributes to homologous recombination repair and chemoresistance in breast cancer. Cellular signalling 8 38522807
2023 Transcription factor E2F8 is a therapeutic target in the basal-like subtype of breast cancer. Frontiers in oncology 8 36814821
2023 Carmofur prevents cell cycle progression by reducing E2F8 transcription in temozolomide-resistant glioblastoma cells. Cell death discovery 8 38086808
2019 Integrated analysis of 10 lymphoma datasets identifies E2F8 as a key regulator in Burkitt's lymphoma and mantle cell lymphoma. American journal of translational research 8 31396343
2015 INHIBITION OF ERN1 SIGNALING ENZYME AFFECTS HYPOXIC REGULATION OF THE EXPRESSION OF E2F8, EPAS1, HOXC6, ATF3, TBX3 AND FOXF1 GENES IN U87 GLIOMA CELLS. Ukrainian biochemical journal 8 26255341
2007 E2F8 is a nonreceptor activator of heterotrimeric G proteins. Journal of molecular signaling 7 17394670
2024 IGF-I protects porcine granulosa cells from hypoxia-induced apoptosis by promoting homologous recombination repair through the PI3K/AKT/E2F8/RAD51 pathway. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 6 38095232
2023 Cyclosporin A inhibits prostate cancer growth through suppression of E2F8 transcription factor in a MELK‑dependent manner. Oncology reports 6 37888771
2022 MicroRNA-1-3p affects lung adenocarcinoma progression through E2F8 and regulating NF-кB pathway. Cytokine 6 35660716
2019 Identification of E2F8 as a Transcriptional Regulator of Gluconeogenesis in Primary Mouse Hepatocytes. Biochemistry. Biokhimiia 6 31870257
2024 Manzamine A reduces androgen receptor transcription and synthesis by blocking E2F8-DNA interactions and effectively inhibits prostate tumor growth in mice. Molecular oncology 5 38605607
2024 ENO1 promotes trophoblast invasion regulated by E2F8 in recurrent miscarriage. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 5 38661062
2024 E2F8-TPX2 axis regulates glycolysis and angiogenesis to promote progression and reduce chemosensitivity of liver cancer. Cytotechnology 4 39435417
2024 Integrative analysis identifies the atypical repressor E2F8 as a targetable transcriptional activator driving lethal prostate cancer. Oncogene 4 39613933
2023 E2F8 knockdown suppresses cell proliferation and induces cell cycle arrest via Wnt/β-Catenin pathway in ovarian cancer. The Chinese journal of physiology 4 37635486
2024 Transcription Factor E2F8 Activates PDK1-Mediated DNA Damage Repair to Enhance Cisplatin Resistance in Lung Adenocarcinoma. Pharmacology 3 38810606
2025 Mechanism Study of E2F8 Activation of SPC25-Mediated Glutamine Metabolism Promoting Immune Escape in Lung Adenocarcinoma. Immunology 2 39829079
2025 Manzamine A: A promising marine-derived cancer therapeutic for multi-targeted interactions with E2F8, SIX1, AR, GSK-3β, and V-ATPase - A systematic review. European journal of pharmacology 2 39863145
2025 E2F8 Transcriptionally Activates DTL to Promote Endometrial Cancer Progression Via the MAPK Pathway. Reproductive sciences (Thousand Oaks, Calif.) 2 41461624
2024 Genetic variant of the sheep E2F8 gene and its associations with litter size. Animal biotechnology 2 38597900
2024 E2F8 facilitates malignant phenotypes of muscle-invasive bladder cancer via increasing MCM7 expression. Biochemistry and cell biology = Biochimie et biologie cellulaire 2 39601318
2025 E2F8-induced GRPEL2 promoted colorectal cancer progression via targeting TIGAR. Journal of translational medicine 1 40269881
2025 Targeting E2F8 sensitizes gemcitabine-resistant gallbladder cancer to PARP inhibitors by disrupting RRM2-driven DNA repair. Journal of experimental & clinical cancer research : CR 1 41392282
2024 TJP1 suppresses trophoblast cell invasion by expressing E2F8 in the human placenta. Molecular and cellular endocrinology 1 38795825
2026 Transcriptional Activation of EGFL6 by E2F8 Promotes Proliferation, Migration, and Invasion in Endometrial Carcinoma Cell. Biology of the cell 0 41555699
2026 KNTC1 initiates a KNTC1/E2F8/MYC positive feedback loop to facilitate tumorigenesis and enhance chemoresistance in bladder cancer. Journal of experimental & clinical cancer research : CR 0 41639725
2026 PAFAH1B3 promotes gastric cancer progression by enhancing E2F8-mediated transcriptional activation of VEGFA expression. Biochemical pharmacology 0 42140448
2025 Bioinformatics insights into TMPO-AS1-let-7b-5p-ESPL1/E2F8 regulatory axis in breast cancer. Frontiers in cell and developmental biology 0 41268575

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