Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
August 25, 2025Open Access

Targeting FOXA1 and FOXA2 Disrupts the Lineage-Specific Oncogenic Output Program in Prostate Cancer

View Full Paper
Ask AI
Bookmark
Share

Authors

NFNicolo' FormaggioJSJacopo SgrignaniGTGayathri Thillaiyampalam

Discussion

Loading...

Member takes

Overview

Experimental analysis shows FOXA1 and FOXA2 cooperation in cell proliferation in prostate cancer, indicating new therapeutic targets.

Key Points

  • Disruption of FOXA1 and FOXA2 leads to cell cycle arrest in prostate cancer cells, preventing growth and proliferation.
  • Joint loss-of-function of FOXA1 and FOXA2 resulted in elimination of specific oncogenic transcription factors.
  • This observational study highlights a dependency for both AR-positive and AR-negative prostate cancers.
  • New findings indicate potential drug targets for addressing lineage-specific cancer subtypes.

Cite This Study

Formaggio et al. (2025) studied this question.

synapsesocial.com/papers/68af7f407567bf4f94ff615dhttps://doi.org/10.1101/2025.08.21.671500
View Full Paper
Ask AI
Bookmark
Share

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1SOX2 utilizes FOXA1 as a heteromeric transcriptional partner to drive proliferation in therapy-resistant prostate cancer2025 · 2 citations
  2. 2FOXA2 and NKX2-1 Orchestrate Neuroendocrine Lineage Plasticity in Prostate Cancer2025
  3. 3Mapping the FOXA1 Interactome in ER+ Breast Cancer Cells using Proximity Labeling Reveals Novel Interactions with the Orphan Nuclear Receptor NR2C22025
  4. 4Regulation of gene expression by FOXA12025
  5. 5Deep Sequencing Reveals Novel Mutations in Androgen Receptor-Related Genes in Prostate Cancer2025