ReviewCancer letters2024
The role of Hippo/YAP1 in cancer-associated fibroblasts: Literature review and future perspectives.
Review in Cancer letters, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed.
- Oncogenic USP3 promotes hepatocellular carcinoma progression via K11/K48-specific deubiquitination and stabilization of YAP.iScience · 2026Article
- RIBOTAC-mediated degradation of hsa-microRNA-301a-3p suppresses TNBC bone metastasis.Science advances · 2026Article
- BART-spatial unravels biologically significant transcriptional regulators from spatial omics data.bioRxiv : the preprint server for biology · 2026Article
- YAP1 Is a Crucial Nexus in the Tumor Microenvironment.Current medical science · 2026Review
- Galectin-3 promotes FBXL5-dependent ubiquitination and degradation of YAP1 to constrain colorectal cancer growth.Frontiers in immunology · 2026Article
- Research Progress and Future Directions in Immune Cell Crosstalk in the Esophageal Cancer: A Bibliometric Analysis.Journal of inflammation research · 2026Review
- Melanoma and its fibroblastic allies: the emerging importance of CAFs in immune suppression, ECM modulation, and therapy resistance.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Targeting Cancer-Associated Fibroblasts in Prostate Cancer: Recent Advances and Therapeutic Opportunities.Cancers · 2025Review
- Tumor Development in Ulcerative Colitis: Perspectives From Biomechanical Characteristics.Development, growth & differentiation · 2025Review
- Post-translational modifications in anaplastic thyroid carcinoma: biological mechanisms and therapeutic potential.Cancer cell international · 2025Review
- The Role of Tumor Microenvironment in Triple-Negative Breast Cancer and Its Therapeutic Targeting.Cells · 2025Review
- Targeting YAP/TAZ-TEAD signaling as a therapeutic approach in head and neck squamous cell carcinoma.Cancer letters · 2025Article
- COPB2 promotes hepatocellular carcinoma progression through regulation of YAP1 nuclear translocation.Oncology research · 2025Article
- Advances in Tumor Microenvironment and Immunotherapeutic Strategies for Hepatocellular Carcinoma.Oncology research · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Cancer-associated fibroblasts (CAFs) are activated fibroblasts that play a role in numerous malignant phenotypes, including hyperproliferation, invasion, and metastasis. These phenotypes correlate with activity of the Hippo pathway oncoprotein, Yes-associated protein-1 (YAP1), and its paralog, transcriptional coactivator with PDZ-binding motif (TAZ). YAP1/TAZ are normally involved in organ growth, under the regulation of various kinases and upon phosphorylation, are retained in the cytoplasm by chaperone proteins, leading to their proteasomal degradation. In CAFs and tumor cells, however, a lack of YAP1 phosphorylation results in its translocation to the nucleus, binding to TEAD transcription factors, and activation of mitogenic pathways. In this review we summarize the literature discussing the central role of YAP1 in CAF activation, the upstream cues that promote YAP1-mediated CAF activation and extracellular matrix remodeling, and how CAFs mediate tumor-stroma crosstalk to support progression, invasion and metastasis in various cancer models. We further highlight YAP1
Indexed as
Identifiers
What OpenQuestion holds
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.