ArticleNature communications2025
STN1 facilitates metastasis by promoting transcription of EMT-activator ZEB1 in pancreatic cancer.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- ARNTL2 promotes metastatic phenotypes through SERPINE1 transcription in KRAS G12D pancreatic cancer.iScience · 2026Article
- STN1 upregulation promotes PARPi resistance in BRCA2-deficient cancer cells via replication fork protection and suppression of ssDNA gap formation.NAR cancer · 2026Article
- From Ferroptotic Stress to Stemness: TNT-Mediated EMT Plasticity in Cancer Progression.Stem cell reviews and reports · 2026Review
- Targeting the CTBP1-CETP axis overcomes ferroptosis resistance in non-small cell lung cancer by altering lipid accumulation.Clinical and translational medicine · 2026Article
- Transcriptomic network analysis and functional evidence identify a candidate EMT hub signature associated with nasopharyngeal carcinoma progression.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Reprogramming the pancreatic ductal adenocarcinoma microenvironment: a novel integrin-targeted cytotoxin, ProAgio, potentiates chemotherapy.Molecular cancer · 2026Article
- STN1 upregulation promotes PARPi resistance in BRCA2-deficient cancer cells via replication fork protection and suppression of ssDNA gap formation.bioRxiv : the preprint server for biology · 2026Article
- tRNA-derived fragment tRF-24 drives CELF1 phase separation to promote oncogenic splicing in esophageal squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) poses a serious clinical challenge, demanding further exploration of its pathogenesis and therapeutic targets for metastasis, the main cause of mortality. Here, we identify STN1, a CST complex member crucial for maintaining telomere lengths and genome stability, as a key factor in promoting PDAC metastasis. Elevated STN1 levels correlate with poor patient survival, with oncogenic protein HOXB7 as an upstream transcription factor regulating STN1. Utilizing multiple PDAC experimental models, we discover STN1's role in promoting metastasis by functioning as an upstream factor in epithelial-mesenchymal transition (EMT). Our mechanistic evidence suggests that during transcription, STN1 binds to structurally displaced single-stranded DNA flanking the R-loop, recruiting STAT3 to activate ZEB1 transcription independent of its known telomere maintenance function. Notably, STAT3 inhibitors show enhanced efficiency in restraining metastatic potential in STN1-overexpressed PDAC cells, offering a potential therapeutic avenue for targeting metastasis in STN1-overexpressed PDAC patients facing an unfavorable prognosis.
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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.