Affinage

E2F5

Transcription factor E2F5 · UniProt Q15329

Length
346 aa
Mass
37.6 kDa
Annotated
2026-04-28
80 papers in source corpus 29 papers cited in narrative 29 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

E2F5 is a member of the E2F transcription factor family that functions as both a transcriptional repressor and activator, integrating pocket protein-dependent cell cycle control with tissue-specific differentiation programs. E2F5 heterodimerizes with DP proteins to bind E2F DNA recognition sequences, preferentially associates with the pocket protein p130 rather than pRb, and its repressive activity requires p130 co-expression; the E2F4/E2F5 pair is dispensable for cell cycle progression but essential for pocket protein-mediated G1 arrest (PMID:7760804, PMID:7542760, PMID:11030352, PMID:18385796). E2F5 subcellular localization is dynamically regulated by an N-terminal nuclear import signal (residues 1–56) and CRM1-dependent nuclear export (residues 130–154), with nuclear accumulation linked to quiescence and differentiation states (PMID:12089160, PMID:17295207). Beyond cell cycle repression, E2F5 directly activates target gene promoters—including MYCN, dmc1, MMP-2, MMP-9, and TFPI2—often in complex with TFDP1 and the chromatin remodeler BRG1, and controls tissue-specific processes including choroid plexus secretory epithelium maturation, multiciliated cell differentiation, spermatogenesis, and mammary alveolar differentiation (PMID:9553039, PMID:26825228, PMID:32196499, PMID:34746136, PMID:32386317, PMID:39341991).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1995 High

    Identification of E2F5 as a new E2F family member that preferentially binds p130 rather than pRb and requires DP-1 heterodimerization for high-affinity DNA binding established the biochemical framework for a distinct p130-associated E2F subfamily with a regulatable transactivation domain.

    Evidence Yeast two-hybrid, co-immunoprecipitation, DNA binding assays, and transactivation reporter assays across multiple labs

    PMID:7542760 PMID:7760804 PMID:7892279

    Open questions at the time
    • Endogenous chromatin target genes of E2F5 were unknown
    • Whether E2F5 functions as a repressor, activator, or both in vivo was unresolved
    • Post-translational regulation beyond phosphorylation was not explored
  2. 1998 High

    E2F5 knockout mice revealed that E2F5 has a tissue-specific nonproliferative role in choroid plexus secretory function, since loss causes hydrocephalus without cell cycle defects, fundamentally expanding the E2F paradigm beyond cell cycle control.

    Evidence Gene-targeted knockout mouse, electron microscopy of choroid plexus, cell cycle analysis of MEFs

    PMID:9553039

    Open questions at the time
    • Transcriptional targets mediating choroid plexus secretory phenotype were not identified
    • Whether the phenotype reflects E2F5 repression or activation was unclear
    • Redundancy with E2F4 in this tissue was not tested
  3. 2000 High

    E2F4/E2F5 double knockout demonstrated that these factors are dispensable for normal proliferation but required for pocket protein-mediated G1 arrest, defining their primary cell cycle role as mediators of growth arrest rather than promoters of proliferation.

    Evidence Double knockout mouse embryonic fibroblasts, p16INK4a-induced G1 arrest assays

    PMID:11030352

    Open questions at the time
    • Individual contributions of E2F4 vs E2F5 to G1 arrest could not be separated
    • Whether E2F5 actively recruits repressive complexes to target promoters was not shown
    • Mechanism by which pocket protein-E2F5 complexes silence specific genes was unknown
  4. 2002 High

    Mapping of distinct nuclear import (residues 1–56) and CRM1-dependent export (residues 130–154) signals revealed that E2F5 activity is controlled by nucleocytoplasmic shuttling independent of pocket proteins or DP partners, explaining how differentiation cues regulate E2F5 function.

    Evidence In vitro nuclear import assay with digitonin-permeabilized cells, leptomycin B treatment, deletion mutagenesis, immunofluorescence in keratinocytes

    PMID:12089160

    Open questions at the time
    • Kinases or signaling pathways controlling the shuttling switch were not identified
    • Whether CRM1-mediated export is the dominant regulatory mechanism in all cell types was untested
    • Structural basis for NLS and NES recognition was not determined
  5. 2007 Medium

    E2F5 nuclear translocation during Raf/MEK1/ERK-mediated myoblast quiescence, independent of p107/p130 relocalization, established that upstream signaling pathways actively direct E2F5 localization to execute growth arrest programs.

    Evidence Subcellular fractionation, MEK inhibitor treatment, immunofluorescence in satellite cells in vitro and in vivo

    PMID:17295207

    Open questions at the time
    • Direct phosphorylation of E2F5 by ERK or downstream kinases was not demonstrated
    • Whether nuclear E2F5 acts as repressor or activator during quiescence was not resolved
    • Role in quiescence maintenance vs entry was not distinguished
  6. 2008 High

    In vivo transgenic epistasis showed that E2F5 alone cannot repress E2F1/E2F3a-driven proliferation in lens fiber cells; co-expression with p130 is required, proving that p130 is essential for E2F5's repressive function rather than merely permissive.

    Evidence Transgenic mouse cross-mating, BrdU incorporation in lens fiber cells

    PMID:18385796

    Open questions at the time
    • Whether p130-independent E2F5 activation functions exist was not tested
    • Chromatin remodeling complexes recruited by E2F5/p130 were not identified
    • The stoichiometry of E2F5/p130 complexes needed for repression was unclear
  7. 2015 High

    ChIP demonstration that E2F5 directly binds ID1 and HMOX1 promoters to repress them in myoblasts, with epistasis rescue by miR-98/E2F5 double knockdown, established E2F5 as a direct transcriptional repressor of specific differentiation-regulatory genes.

    Evidence ChIP on endogenous promoters, miRNA knockdown, epistasis rescue in skeletal muscle differentiation assay

    PMID:25422988

    Open questions at the time
    • Whether repression involves p130 recruitment at these promoters was not tested
    • Genome-wide direct target repertoire of E2F5 in myoblasts was not mapped
    • Histone modification changes at repressed promoters were not examined
  8. 2016 High

    Conditional E2f4 deletion combined with E2f5 heterozygosity eliminated multiciliated cells in male efferent ducts, establishing that E2F4/E2F5 cooperatively control multiciliated cell differentiation in vivo beyond the choroid plexus.

    Evidence Conditional knockout mouse (Vil-cre), immunohistochemistry, reproductive phenotype analysis

    PMID:26825228

    Open questions at the time
    • Direct transcriptional targets of E2F5 driving multiciliogenesis were not identified
    • Relative contributions of E2F4 vs E2F5 to ciliogenesis program were not separated
    • Whether E2F5 activates or represses ciliogenesis genes was not determined
  9. 2020 High

    ChIP and mutagenesis demonstrated that E2F5 directly occupies TFPI2, MMP-2, and MMP-9 promoters with opposing transcriptional outcomes (repression vs activation), and zebrafish genetics showed E2F5 directly activates dmc1 for meiotic recombination, establishing E2F5 as a context-dependent dual-function transcription factor at specific target loci.

    Evidence ChIP with qPCR, site-directed mutagenesis of luciferase reporters, zymography for MMP activity; zebrafish mutant genetics with dmc1 rescue and ChIP

    PMID:32196499 PMID:32386317

    Open questions at the time
    • What determines whether E2F5 activates or represses at a given promoter was unknown
    • Whether cofactor composition (e.g., p130 vs BRG1) dictates activation vs repression was not tested at these loci
    • Structural basis for E2F5 binding specificity at non-canonical promoters was not addressed
  10. 2021 High

    Discovery that E2F5 forms a complex with TFDP1 and the chromatin remodeler BRG1 to activate MYCN transcription via H3 acetylation and H3K4me3 at the MYCN promoter provided the first mechanistic explanation for E2F5's activator function through chromatin remodeling cofactor recruitment.

    Evidence Co-IP, ChIP for E2F5/TFDP1/BRG1 at MYCN promoter, histone modification analysis, reporter assays in hepatocytes

    PMID:34746136

    Open questions at the time
    • Whether BRG1 recruitment is specific to activator targets or also occurs at repressed loci was not tested
    • The switch mechanism between repressive (p130) and activating (BRG1) complex assembly was not defined
    • Genome-wide mapping of E2F5/BRG1 co-occupancy was not performed
  11. 2022 Medium

    Post-transcriptional regulation of E2F5 was established through METTL3-mediated m6A methylation stabilizing E2F5 mRNA, and IMP3 binding to E2F5 mRNA extending its half-life, revealing that E2F5 expression is controlled at the RNA level by epitranscriptomic and RNA-binding protein mechanisms.

    Evidence MeRIP assay, RIP assay, mRNA half-life measurement, siRNA knockdown with rescue in pancreatic cancer and oral squamous cell carcinoma cells

    PMID:35985439 PMID:38271139

    Open questions at the time
    • Specific m6A sites on E2F5 mRNA were not mapped at nucleotide resolution
    • Whether METTL3 and IMP3 act on the same or different E2F5 mRNA regions was not determined
    • Physiological contexts beyond cancer where this regulation operates were not tested
  12. 2024 High

    Mammary-specific E2F5 conditional knockout demonstrated that E2F5 promotes alveolar differentiation during pregnancy by maintaining H3K27me3 repression at luminal progenitor genes, and its long-term loss leads to metastatic mammary tumors, revealing E2F5 as a chromatin-level coordinator of mammary cell fate with tumor suppressive function.

    Evidence Conditional knockout mouse, scRNAseq, RNAseq, H3K27me3 ChIP, tumor transplantation, whole genome sequencing

    PMID:39341991

    Open questions at the time
    • Whether E2F5 directly recruits PRC2 to deposit H3K27me3 or acts indirectly was not established
    • The specific mutations driving tumorigenesis after E2F5 loss were not fully characterized
    • Whether the tumor suppressive function is p130-dependent was not tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • The molecular mechanism determining whether E2F5 acts as a repressor (via p130) or activator (via BRG1/TFDP1) at a given target promoter, and how upstream signals switch between these modes, remains the central unresolved question in E2F5 biology.
  • No genome-wide ChIP-seq map of E2F5 occupancy with concurrent cofactor binding exists
  • Structural basis for E2F5 interaction with p130 vs BRG1 is not resolved
  • Whether E2F5 directly recruits PRC2 for H3K27me3 deposition at progenitor genes is unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 7 GO:0003677 DNA binding 5
Localization
GO:0005634 nucleus 4 GO:0005829 cytosol 2
Pathway
R-HSA-74160 Gene expression (Transcription) 6 R-HSA-1640170 Cell Cycle 4 R-HSA-1266738 Developmental Biology 3 R-HSA-4839726 Chromatin organization 2
Partners
CDK13IGF2BP3RBL2SMARCA4TFDP1
Complex memberships
E2F5/TFDP1/BRG1 activating complexE2F5/p130 repressive complex

Evidence

Reading pass · 29 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 E2F-5 was identified as a new E2F family member that interacts preferentially with p130 (not pRb) under physiological conditions, as demonstrated by yeast two-hybrid assay and co-immunoprecipitation with specific E2F-5 antiserum. Yeast two-hybrid assay, co-immunoprecipitation with specific antiserum Molecular and cellular biology High 7760804
1995 E2F-5 heterodimerizes with DP-1 to acquire high-affinity E2F DNA recognition sequence binding, and its C-terminal transactivation domain is specifically inactivated upon pocket protein binding. Yeast two-hybrid, DNA binding assays, transactivation reporter assays in yeast and mammalian cells Oncogene High 7542760
1995 E2F-4 and E2F-5 interact with p130 (not pRb) in yeast two-hybrid assays and fail to bind pRb, defining them as a distinct E2F subfamily; E2F-4 and E2F-5 mRNA expression peaks in mid-G1 phase before E2F-1 expression. Yeast two-hybrid, synchronized keratinocyte expression analysis Proceedings of the National Academy of Sciences of the United States of America High 7892279
1995 E2F-5 protein is expressed as multiple species (46–54 kDa) as a result of differential phosphorylation, and contains a strong transactivation domain at the C-terminal region (amino acids 273–346). Western blot, deletion mapping, reporter gene assays Biochemical and biophysical research communications Medium 9464260
1998 E2F-5 knockout mice develop nonobstructive hydrocephalus associated with excessive CSF secretory activity in choroid plexus epithelium, while cell cycle kinetics are not perturbed in knockout embryo fibroblasts, indicating E2F-5 has a nonproliferative, tissue-specific role in choroid plexus secretory function. Gene targeting/knockout mouse model, electron microscopy, cell cycle analysis Genes & development High 9553039
2000 Simultaneous inactivation of E2F4 and E2F5 in mice results in failure to arrest in G1 in response to p16INK4a, demonstrating that E2F4 and E2F5 are dispensable for cell cycle progression but necessary for pocket protein-mediated G1 arrest. Double knockout mouse genetics, embryonic fibroblast cell cycle analysis Molecular cell High 11030352
2000 E2F5 can cooperate with DP1 and activated RAS to promote morphological transformation in primary baby rat kidney cells, behaving as a MYC-type cooperating oncogene, and the human E2F5 gene is amplified at 8q21.1-21.3 in breast tumors. Focus formation assay in BRK cells, gene mapping, copy number analysis in 442 breast tumor DNAs Genes, chromosomes & cancer High 10738311
2002 E2F-5 nuclear import requires only the first N-terminal 56 amino acid residues and is independent of DP or pRB family proteins; nuclear export is mediated through CRM1 (leptomycin B-sensitive) via amino acid residues 130–154, excluding DNA- and p130-binding domains, and keratinocyte differentiation shifts E2F-5 localization from cytoplasm to nucleus. In vitro nuclear import assay with digitonin-permeabilized cells, leptomycin B treatment, deletion mutagenesis, immunofluorescence The Journal of biological chemistry High 12089160
2005 In mouse and human choroid plexus epithelium, E2F5 protein shifts from predominantly nuclear (early development) to cytoplasmic localization late in embryogenesis, coinciding with morphological maturation from pseudostratified to cuboidal epithelium, but not with proliferating cell status. Immunohistochemistry, in situ hybridization, PCNA co-staining in developing mouse and human tissues The International journal of developmental biology Medium 16172982
2006 E2F-5 is upregulated during euxanthone-induced neurite outgrowth via the PKC pathway, and siRNA-mediated gene silencing of E2F-5 abolishes euxanthone-induced neurite outgrowth in neuroblastoma cells. 2D gel electrophoresis/MALDI-ToF proteomics, PKC inhibitor (Go6976) treatment, siRNA knockdown, neurite outgrowth assay The international journal of biochemistry & cell biology Medium 16546434
2007 E2F5 and LEK1 translocate to the nucleus as an early event during Raf kinase-mediated myoblast quiescence, dependent on MEK1/ERK signaling; MEK1 inhibition prevents nuclear translocation of E2F5 while pocket proteins p107 and p130 remain cytoplasmic. Proteomics (2D gel), subcellular fractionation, MEK inhibitor treatment, immunofluorescence of satellite cells in vitro and in vivo Journal of cellular biochemistry Medium 17295207
2008 Overexpression of E2F5 alone is insufficient to inhibit E2F1 or E2F3a-induced cell cycle reentry in lens fiber cells in vivo; co-expression of E2F5 with p130 (E2F5/p130 complex) is required to reduce BrdU-positive proliferating cells, demonstrating that p130 is essential for E2F5 repressive activity. Transgenic mouse generation, cross-mating, BrdU incorporation assay, immunohistochemistry Molecular vision High 18385796
2010 E2F5 acts as a direct transcriptional activator of HPV18 E6/E7 oncogenes in HeLa cells by binding E2F sites specific to HPV18, and E2F5 positively regulates S-phase entry in HPV18-expressing cells, converting its role from repressor to activator. Sequential siRNA silencing of E2F family members, promoter analysis, ChIP (implied by binding site validation), cell cycle analysis Oncogene Medium 20639900
2011 miR-128-2 post-transcriptionally targets E2F5 mRNA, leading to abrogation of E2F5 repressive activity on p21waf1 transcription; resulting cytoplasmic p21waf1 prevents pro-caspase-3 cleavage, conferring chemoresistance in non-small-cell lung cancer. miRNA target validation (western blot, luciferase reporter), siRNA, cell viability assays Cell death and differentiation Medium 22193543
2015 E2F5 directly binds to the promoters of ID1 (inhibitor of DNA binding 1) and HMOX1 and represses their expression in skeletal myoblasts; miR-98 targets E2F5 to regulate skeletal muscle differentiation, and knockdown of both miR-98 and E2F5 restores normal differentiation. Transcriptomics, miRNA knockdown, ChIP on ID1 and HMOX1 promoters, epistasis rescue experiment The Biochemical journal High 25422988
2016 E2F5 overexpression is accompanied by higher phosphorylation of SMAD3 at Ser-208 linker region (pSMAD3L) and p38 in prostate cancer; downregulation of E2F5 and p38 in PC3 cells reduces SMAD3 phosphorylation and causes G1 arrest, establishing a deregulated E2F5/p38/SMAD3 axis driving uncontrolled proliferation. siRNA knockdown, qRT-PCR, western blot, immunohistochemistry, cell cycle analysis Journal of cellular physiology Medium 26919443
2016 E2f4 and E2f5 control multiciliated cell differentiation and fluid absorption in male efferent ducts; conditional E2f4 deletion in Vil-cre mice combined with E2f5 heterozygosity eliminates multiciliated cells and reduces aquaporin1 and clusterin expression, leading to sperm accumulation and male sterility. Conditional knockout mouse (Vil-cre), immunohistochemistry, histology, reproductive phenotype analysis Cell cycle (Georgetown, Tex.) High 26825228
2019 E2F5 directly binds to the promoter of lncPCAT1 to drive its transcription, forming a feed-forward regulatory loop in which lncPCAT1 sponges miR-106a-5p to derepress BMP2 and E2F5 itself, promoting osteogenic differentiation of periodontal ligament stem cells. ChIP, luciferase reporter assay, miRNA/lncRNA interaction assays, osteogenic differentiation assays in vitro and in vivo Journal of cellular physiology Medium 30997692
2019 MYCN directly binds to a Myc E-Box motif within the E2F5 gene promoter to induce its transcription; E2F5 knockdown inhibits neuroblastoma cell proliferation and cell cycle progression, accompanied by reduced CDK2 and CDK6 expression. ChIP, luciferase reporter assay, siRNA knockdown, cell cycle analysis Biochemical and biophysical research communications Medium 30765227
2020 E2F5 directly occupies the promoters of TFPI2, MMP-2, and MMP-9 as confirmed by ChIP and site-directed mutagenesis of luciferase reporters; E2F5 represses TFPI2 while activating MMP-2 and MMP-9, promoting prostate cancer cell migration and invasion. Artemisinin treatment represses E2F5 to restore this axis. ChIP with anti-E2F5-IgG plus qPCR, site-directed mutagenesis, dual-luciferase assay, Proteome Profiler array, gelatin zymography, co-immunoprecipitation in tissue Carcinogenesis High 32386317
2020 E2F5 knockdown in breast cancer MCF7 cells (wild-type TP53) triggers cell death by upregulating TP53 target genes BAX, NOXA, and PUMA; this effect is abrogated by TP53 silencing, while E2F5 knockdown in TP53-mutant cells (MDA-MB-231, BT474) does not induce apoptosis. siRNA knockdown, TP53 silencing, qRT-PCR for apoptosis-related genes, proliferation assay Oncology reports Medium 33000282
2020 Zebrafish E2f5 functions as a transcriptional activator of dmc1 (meiotic recombination protein) by binding to its promoter; loss of e2f5 arrests spermatogenesis at zygotene stage due to homologous recombination defects, and overexpression of dmc1 rescues fertility in e2f5 mutants. E2f5 also activates Notch pathway gene jagged2b to inhibit MCC fate in neighboring cells. Zebrafish genetics (mutant, double mutant), transcriptome analysis, ChIP on dmc1 promoter, dmc1 rescue experiment, Notch pathway analysis PLoS genetics High 32196499
2021 CDK13 interacts with E2F5 protein (identified by Co-IP coupled with mass spectrometry) and strengthens its pro-proliferative effect; CDK13 transcriptional activation promotes E2F5 protein expression via circCDK13 formation which sponges miR-212-5p/449a, and E2F5 in turn enhances CDK13 transcription, forming a positive feedback loop. Co-immunoprecipitation with mass spectrometry, CRISPR-Cas9 endogenous activation, gain/loss-of-function assays, luciferase assays Journal of experimental & clinical cancer research : CR Medium 33390186
2021 E2F5 forms a complex with TFDP1 and BRG1 (chromatin remodeling protein) to transcriptionally activate MYCN in hepatocytes during liver regeneration; BRG1 is recruited by E2F5/TFDP1 to the MYCN promoter and facilitates histone H3 acetylation and H3K4 trimethylation to promote RNA Pol II binding. RNA interference, ChIP, Co-IP, histone modification analysis, reporter assays, hepatocyte proliferation assay Frontiers in cell and developmental biology High 34746136
2021 E2F5 directly upregulates UBE2T transcription in gastric cancer; E2F5 knockdown inhibits proliferation and invasion, and UBE2T overexpression rescues these effects, establishing an E2F5/UBE2T transcriptional axis. siRNA knockdown, GSEA, correlation analysis, rescue experiments Digestive and liver disease Medium 34583905
2022 METTL3 promotes E2F5 mRNA stability through m6A methylation of E2F5; METTL3 knockdown decreases E2F5 protein expression and inhibits pancreatic cancer cell viability and invasion, effects rescued by E2F5 overexpression. MeRIP assay (m6A measurement), siRNA knockdown, rescue overexpression, CCK-8, wound healing, transwell, xenograft Cellular signalling Medium 35985439
2024 RNA-binding protein IMP3 binds E2F5 mRNA (confirmed by RIP assay) and stabilizes it; IMP3 silencing shortens E2F5 mRNA half-life, reduces E2F5 protein expression, and inhibits oral squamous cell carcinoma cell proliferation and xenograft tumor growth. RNA immunoprecipitation (RIP), siRNA knockdown, mRNA half-life assay, xenograft model Aging Medium 38271139
2024 Mammary-specific E2F5 conditional knockout leads to delayed alveolar expansion during early pregnancy with reduced expression of canonical E2F target cell cycle genes, enrichment of luminal progenitor populations at expense of differentiated alveolar cells, and depletion of repressive H3K27me3 at luminal progenitor-associated genes; after prolonged latency, knockout mice develop highly metastatic mammary tumors with altered Cyclin D1 levels. Conditional knockout mouse, scRNAseq, RNAseq, chromatin profiling (H3K27me3), tumor transplantation, whole genome sequencing, western blot Oncogene High 39341991
2024 E2F5 chromatin binding increases during early pregnancy in mammary gland; E2F5 deletion leads to reduced H3K27me3 at luminal progenitor-associated genes, suggesting E2F5 normally coordinates repression of progenitor programs to promote differentiation into proliferative alveolar precursors. Conditional knockout, chromatin profiling (H3K27me3 ChIP), scRNAseq, ATAC-seq (implied by chromatin binding data) bioRxivpreprint Medium bio_10.1101_2024.11.27.625731

Source papers

Stage 0 corpus · 80 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1995 E2F-4 and E2F-5, two members of the E2F family, are expressed in the early phases of the cell cycle. Proceedings of the National Academy of Sciences of the United States of America 326 7892279
2000 E2F4 and E2F5 play an essential role in pocket protein-mediated G1 control. Molecular cell 236 11030352
1995 E2F-5, a new E2F family member that interacts with p130 in vivo. Molecular and cellular biology 223 7760804
1998 A specific, nonproliferative role for E2F-5 in choroid plexus function revealed by gene targeting. Genes & development 153 9553039
2017 SNHG16 contributes to breast cancer cell migration by competitively binding miR-98 with E2F5. Biochemical and biophysical research communications 139 28232182
2011 MicroRNA-128-2 targets the transcriptional repressor E2F5 enhancing mutant p53 gain of function. Cell death and differentiation 134 22193543
2018 The putative tumour suppressor miR-1-3p modulates prostate cancer cell aggressiveness by repressing E2F5 and PFTK1. Journal of experimental & clinical cancer research : CR 65 30185212
1995 Molecular and functional characterisation of E2F-5, a new member of the E2F family. Oncogene 52 7542760
2016 The transcription factor FOXN3 inhibits cell proliferation by downregulating E2F5 expression in hepatocellular carcinoma cells. Oncotarget 51 27259277
2016 MicroRNA-154 inhibits growth and invasion of breast cancer cells through targeting E2F5. American journal of translational research 50 27398145
2014 Up-regulated MicroRNA-181a induces carcinogenesis in hepatitis B virus-related hepatocellular carcinoma by targeting E2F5. BMC cancer 50 24529171
2016 E2f4 and E2f5 are essential for the development of the male reproductive system. Cell cycle (Georgetown, Tex.) 48 26825228
2021 CDK13 upregulation-induced formation of the positive feedback loop among circCDK13, miR-212-5p/miR-449a and E2F5 contributes to prostate carcinogenesis. Journal of experimental & clinical cancer research : CR 47 33390186
2019 Long noncoding RNA SNHG6 functions as a competing endogenous RNA by sponging miR-181a-5p to regulate E2F5 expression in colorectal cancer. Cancer management and research 46 30666158
2011 A potential oncogenic role of the commonly observed E2F5 overexpression in hepatocellular carcinoma. World journal of gastroenterology 46 21274376
2009 Overexpression of E2F-5 correlates with a pathological basal phenotype and a worse clinical outcome. British journal of cancer 43 19259095
2016 miR-132 targeting E2F5 suppresses cell proliferation, invasion, migration in ovarian cancer cells. American journal of translational research 40 27186275
2015 MicroRNA-34a targets FMNL2 and E2F5 and suppresses the progression of colorectal cancer. Experimental and molecular pathology 40 26103003
2010 E2F5 status significantly improves malignancy diagnosis of epithelial ovarian cancer. BMC cancer 40 20181230
2000 Human E2F5 gene is oncogenic in primary rodent cells and is amplified in human breast tumors. Genes, chromosomes & cancer 40 10738311
2017 MiR-613 suppresses retinoblastoma cell proliferation, invasion, and tumor formation by targeting E2F5. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 38 28351331
2018 MicroRNA-1179 inhibits the proliferation, migration and invasion of human pancreatic cancer cells by targeting E2F5. Chemico-biological interactions 37 29859832
2018 Induction of apoptosis in ovarian cancer cells by miR-493-3p directly targeting AKT2, STK38L, HMGA2, ETS1 and E2F5. Cellular and molecular life sciences : CMLS 37 30392041
2019 A feed-forward regulatory network lncPCAT1/miR-106a-5p/E2F5 regulates the osteogenic differentiation of periodontal ligament stem cells. Journal of cellular physiology 36 30997692
2016 miRNA-154-5p Inhibits Proliferation, Migration and Invasion by Targeting E2F5 in Prostate Cancer Cell Lines. Urologia internationalis 36 27074041
2002 Active nuclear import and export pathways regulate E2F-5 subcellular localization. The Journal of biological chemistry 36 12089160
2020 E2f5 is a versatile transcriptional activator required for spermatogenesis and multiciliated cell differentiation in zebrafish. PLoS genetics 34 32196499
2018 MicroRNA-129-3p suppresses tumor growth by targeting E2F5 in glioblastoma. European review for medical and pharmacological sciences 34 29509253
2020 E2F5 promotes prostate cancer cell migration and invasion through regulation of TFPI2, MMP-2 and MMP-9. Carcinogenesis 31 32386317
2020 Circular RNA ABCB10 promotes non-small cell lung cancer progression by increasing E2F5 expression through sponging miR-584-5p. Cell cycle (Georgetown, Tex.) 31 32420810
2013 Effects of microRNA-106 on proliferation of gastric cancer cell through regulating p21 and E2F5. Asian Pacific journal of cancer prevention : APJCP 29 23803041
2018 Distinct requirements of E2f4 versus E2f5 activity for multiciliated cell development in the zebrafish embryo. Developmental biology 28 30218642
2017 miRNA-34a enhances the sensitivity of gastric cancer cells to treatment with paclitaxel by targeting E2F5. Oncology letters 28 28599485
2020 LncRNA MALAT1 Regulates the Progression and Cisplatin Resistance of Ovarian Cancer Cells via Modulating miR-1271-5p/E2F5 Axis. Cancer management and research 26 33116856
2016 Deregulated E2F5/p38/SMAD3 Circuitry Reinforces the Pro-Tumorigenic Switch of TGFβ Signaling in Prostate Cancer. Journal of cellular physiology 24 26919443
2005 Changes in E2F5 intracellular localization in mouse and human choroid plexus epithelium with development. The International journal of developmental biology 23 16172982
2013 Analysis of genetic aberrations on chromosomal region 8q21-24 identifies E2F5 as an oncogene with copy number gain in prostate cancer. Medical oncology (Northwood, London, England) 22 23377984
2022 METTL3 promotes the growth and metastasis of pancreatic cancer by regulating the m6A modification and stability of E2F5. Cellular signalling 19 35985439
2021 CircFAM13B promotes the proliferation of hepatocellular carcinoma by sponging miR-212, upregulating E2F5 expression and activating the P53 pathway. Cancer cell international 19 34348712
2019 MYCN-induced E2F5 promotes neuroblastoma cell proliferation through regulating cell cycle progression. Biochemical and biophysical research communications 17 30765227
2006 Involvement of protein kinase C and E2F-5 in euxanthone-induced neurite differentiation of neuroblastoma. The international journal of biochemistry & cell biology 16 16546434
2015 miR-98 delays skeletal muscle differentiation by down-regulating E2F5. The Biochemical journal 15 25422988
2021 Downregulation of long non-coding RNA UCA1 represses tumorigenesis and metastasis of osteosarcoma via miR-513b-5p/E2F5 axis. Anti-cancer drugs 14 33595944
2019 miR‑132 inhibits high glucose‑induced vascular smooth muscle cell proliferation and migration by targeting E2F5. Molecular medicine reports 14 31257477
2010 The E2F5 repressor is an activator of E6/E7 transcription and of the S-phase entry in HPV18-associated cells. Oncogene 14 20639900
2021 An E2F5-TFDP1-BRG1 Complex Mediates Transcriptional Activation of MYCN in Hepatocytes. Frontiers in cell and developmental biology 13 34746136
2018 Let-7c Inhibits the Proliferation, Invasion, and Migration of Glioma Cells via Targeting E2F5. Oncology research 13 29362021
2007 E2F5 and LEK1 translocation to the nucleus is an early event demarcating myoblast quiescence. Journal of cellular biochemistry 13 17295207
1998 The molecular and functional characterization of E2F-5 transcription factor. Biochemical and biophysical research communications 13 9464260
2021 E2F5 promotes proliferation and invasion of gastric cancer through directly upregulating UBE2T transcription. Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver 12 34583905
2008 Thyroid hormone - triiodothyronine - has contrary effect on proliferation of human proximal tubules cell line (HK2) and renal cancer cell lines (Caki-2, Caki-1) - role of E2F4, E2F5 and p107, p130. Thyroid research 12 19014670
2020 MicroRNA-1271-5p inhibits the tumorigenesis of ovarian cancer through targeting E2F5 and negatively regulates the mTOR signaling pathway. Panminerva medica 11 32414231
1995 Structural characterization and specificity of expression of E2F-5: a new member of the E2F family of transcription factors. Cellular & molecular biology research 11 8589754
2021 Targeting CALM2 Inhibits Hepatocellular Carcinoma Growth and Metastasis by Suppressing E2F5-mediated Cell Cycle Progression. Anticancer research 10 33788723
2023 MAPK Is a Mutual Pathway Targeted by Anxiety-Related miRNAs, and E2F5 Is a Putative Target for Anxiolytic miRNAs. Biomolecules 9 36979479
2023 LINC01980 induced by TGF-beta promotes hepatocellular carcinoma metastasis via miR-376b-5p/E2F5 axis. Cellular signalling 9 37827344
2022 CircFOXM1 promotes the proliferation, migration, invasion, and glutaminolysis of glioblastoma by regulating the miR-577/E2F5 axis. Bosnian journal of basic medical sciences 8 34784267
2008 Overexpression of E2F5/p130, but not E2F5 alone, can inhibit E2F-induced cell cycle entry in transgenic mice. Molecular vision 8 18385796
2020 Knockdown of E2F5 induces cell death via the TP53‑dependent pathway in breast cancer cells carrying wild‑type TP53. Oncology reports 7 33000282
2021 E2F5 Promotes the Malignancy of Ovarian Cancer Via the Regulation of Hippo and Wnt Pathways. Genetic testing and molecular biomarkers 6 33734894
2021 Inhibition of HDACs Suppresses Cell Proliferation and Cell Migration of Gastric Cancer by Regulating E2F5 Targeting BCL2. Life (Basel, Switzerland) 6 34947956
2001 [Differences in human and rat FSH receptors promote activity as a result of the transcriptional factors: E2F1, E2F4 and E2F5 overexpression]. Ginekologia polska 6 11883315
2019 MicroRNA‑34a inhibits esophageal squamous cell carcinoma progression by targeting E2F5. Journal of B.U.ON. : official journal of the Balkan Union of Oncology 5 31983127
2023 E2F5 Targeted by Let-7d-5p Facilitates Cell Proliferation, Metastasis and Immune Escape in Gallbladder Cancer. Digestive diseases and sciences 4 38087129
2022 hsa_circ_0084811 Regulates Cell Proliferation and Apoptosis in Retinoblastoma through miR-18a-5p/miR-18b-5p/E2F5 Axis. BioMed research international 4 35909488
2016 Aberrant Promoter Methylation at CpG Cytosines Induce the Upregulation of the E2F5 Gene in Breast Cancer. Journal of breast cancer 4 27382388
2024 Insight into mammary gland development and tumor progression in an E2F5 conditional knockout mouse model. Oncogene 3 39341991
2009 Identification and expression analysis of two zebrafish E2F5 genes during oogenesis and development. Molecular biology reports 3 19578977
2024 Knockdown of RNA-binding protein IMP3 suppresses oral squamous cell carcinoma proliferation by destabilizing E2F5 transcript. Aging 1 38271139
2024 Retracted: hsa_circ_0084811 Regulates Cell Proliferation and Apoptosis in Retinoblastoma through miR-18a-5p/miR-18b-5p/E2F5 Axis. BioMed research international 1 38550126
2023 [Effects of lncRNA SNHG12 on the proliferation, migration and invasiveness of prostate cancer cells by regulating E2F5 expression]. Zhonghua nan ke xue = National journal of andrology 1 37847082
2026 Crosstalk Between FOXN3 and E2F5 Reveals a Novel Tumor Suppressive Pathway in Acute Myeloid Leukemia via MAPK Signaling: Implications for Potential Future Targeted Therapy. Blood and lymphatic cancer : targets and therapy 0 41908971
2026 E2F5 Promotes Vascular Endothelial Cell Proliferation and Angiogenesis in Diabetic Lower Limb Ischemia via an Autophagy-Related Mechanism. Circulation journal : official journal of the Japanese Circulation Society 0 41987367
2025 Investigating the clinical significance of E2F5 expression in circulating extracellular vesicles in prostate carcinoma. Urologia 0 39907045
2025 E2F5 Accelerates Vascular Smooth Muscle Cells Phenotype Switching in Diabetic Atherosclerosis through Activating Wnt/β-Catenin Pathway. Diabetes & metabolism journal 0 40890020
2025 circ_0000132 Regulates Chicken Granulosa Cell Proliferation Apoptosis and E2/P4 Synthesis via miR-206 E2F5 Signaling. International journal of molecular sciences 0 41226814
2025 E2F5 Overexpression in Laryngeal Squamous Cell Carcinoma: Associations With Neutrophil Extracellular Traps in the Tumor Microenvironment. World journal of oncology 0 41488283
2025 Fu Zheng Xiao Yu San Jie Decoction affects the proliferation of renal cell carcinoma via regulating E2F5 gene. Translational andrology and urology 0 41522321
2023 Long Noncoding RNA SNHG6 Functions as a Competing Endogenous RNA by Sponging miR-181a-5p to Regulate E2F5 Expression in Colorectal Cancer [Retraction]. Cancer management and research 0 37228644
2022 miR-132 targeting E2F5 suppresses cell proliferation, invasion, migration in ovarian cancer cells [Retraction]. American journal of translational research 0 35173889