ArticleCell death discovery2025
CREB5 promotes nodal metastasis of cervical cancer by regulation of APLN-induced lymphangiogenesis.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The trial behind it
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Who cites it
4 citing papers in PubMed.
- Lymphatic Endothelial Cells in Health and Disease.MedComm · 2026Review
- Xanthatin Attenuates Angiotensin II-Induced Cardiac Hypertrophy by Targeting CREB5.Journal of cardiovascular translational research · 2026Article
- Lymphangiogenesis-related gene signature-based risk model for prognostic assessment of cervical cancer: immune-metabolic characterization and molecular subtype analysis.Frontiers in genetics · 2026Article
- Single-cell atlas reveals a pro-metastatic RELB+ neutrophil-myeloid subset underlying lymph node metastasis in EGFR-wildtype LUAD.Frontiers in cell and developmental biology · 2026Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Lymph node metastasis (LNM), a hallmark of aggressive cervical cancer (CCa), severely compromises prognosis and limits therapeutic efficacy. Despite its clinical significance, the molecular mechanisms driving LNM in CCa remain poorly characterized, necessitating urgent exploration. In this study, leveraging an in vitro lymphangiogenesis screening model, we identified CREB5 as a gene markedly upregulated in metastatic CCa, with its expression strongly correlating with LNM and poor patient survival. Mechanistic investigations revealed that CREB5 transcriptionally activates apelin (APLN) by directly binding to its canonical TGACG motif in the promoter region, thereby driving APLN-mediated lymphangiogenesis. Inhibition of CREB5 or treatment with ML221, a selective APLN receptor (APLNR) antagonist, potently suppressed lymphatic metastasis in preclinical CCa models. These findings establish CREB5 as a critical regulator of APLN-dependent lymphangiogenesis and LNM, highlighting its potential as a dual diagnostic biomarker and therapeutic target for mitigating lymphatic dissemination in CCa patients.
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Registered trials
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