ArticleOncogene2025
Integrative analysis identifies the atypical repressor E2F8 as a targetable transcriptional activator driving lethal prostate cancer.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- CRISPR decodes the RNA regulatory network in prostate cancer: A review from mechanisms to precision therapeutics.Non-coding RNA research · 2026Review
- E2F-mediated activation of mTORC1 through the ubiquitin-proteasome system promotes lung adenocarcinoma progression.Cell death & disease · 2026Article
- Chronobiology of neurotropic viruses: rhythmic viral entry and arrhythmic host clocks.Cell discovery · 2026Article
- Emerging therapies to overcome antiandrogen resistance and beyond in lethal prostate cancer.Journal of the National Cancer Center · 2026Review
- A Platform-Independent Binary Gene-Pair Signature Derived from CRPC-Enriched Single-Cell Transcriptomics for Predicting Recurrence-Free Survival in Prostate Cancer.Cancer management and research · 2026Article
- Targeting E2F8 sensitizes gemcitabine-resistant gallbladder cancer to PARP inhibitors by disrupting RRM2-driven DNA repair.Journal of experimental & clinical cancer research : CR · 2025Article
- Enhanced RNA-targeting CRISPR-Cas technology in zebrafish.Nature communications · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Acquired resistance to androgen receptor (AR)-targeted therapies underscores the need to identify alternative therapeutic targets for treating lethal prostate cancer. In this study, we evaluated the prognostic significance of 1635 human transcription factors (TFs) by analyzing castration-resistant prostate cancer (CRPC) datasets from the West and East Stand Up to Cancer (SU2C) cohorts. Through this screening approach, we identified E2F8, a putative transcriptional repressor, as a TF consistently associated with poorer patient outcomes in both cohorts. Notably, E2F8 is highly expressed and active in AR-negative CRPC compared to AR-positive CRPC. Integrative profiling of E2F8 cistromes and transcriptomes in AR-negative CRPC cells revealed that E2F8 directly and non-canonically activates target oncogenes involved in cancer-associated pathways. To target E2F8 in CRPC, we employed the CRISPR/CasRx system to knockdown E2F8 mRNA, resulting in effective and specific downregulation of E2F8 and its target oncogenes, as well as significant growth inhibition in AR-negative CRPC in both cultured cells and xenograft models. Our findings identify and characterize E2F8 as a targetable transcriptional activator driving CRPC, particularly the growth of AR-negative CRPC.
Indexed as
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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.