ArticleSignal transduction and targeted therapy2025
Dysadherin/YAP axis fuels stem plasticity and immune escape in liver cancer.
Article in Signal transduction and targeted therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Nanomedicine targeting ECM stiffness: restoring mechanical homeostasis for cancer immunotherapy.Materials today. Bio · 2026Review
- Biomimetic nanodecoys remodel the mechano-immune microenvironment to potentiate checkpoint blockade in colorectal cancer.Journal of nanobiotechnology · 2026Article
- Circular RNAs as molecular bridges: dual regulation of ferroptosis and immunity in cancer.Frontiers in immunology · 2026Review
- Spatiotemporal control of mitoribosome-mediated metabolic reprogramming in cancer: implications for heterogeneity and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
- Engineered CAR-T extracellular vesicles loaded with miR-17-5p inhibitor suppress hepatocellular carcinoma progression.Frontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Hepatocellular carcinoma (HCC) is an aggressive malignancy that is often refractory to chemotherapy and immune checkpoint inhibitors. This therapeutic resistance is driven in part by the persistence of cancer stem-like cells (CSCs) and the development of an immune-cold tumor microenvironment. However, the upstream regulators that coordinate these malignant features remain poorly defined. In this study, we identified dysadherin as a novel upstream activator of YAP that promotes both CSC plasticity and immune evasion through the FAK/YAP/TEAD2 signaling axis. Using single-cell transcriptomic analysis, in vitro assays, and multiple in vivo models including a humanized immune mouse system, we showed that dysadherin enhances the expression of pluripotency genes, such as OCT4 and upregulates PD-L1. These changes support stem-like tumor behavior and contribute to T-cell exclusion, fostering an immunosuppressive niche. Notably, genetic knockdown or peptide-based pharmacologic inhibition of dysadherin effectively restored antitumor immune activation, suppressed metastasis and improved therapeutic responsiveness. Our findings reveal a mechanistic link between dysadherin-mediated cell adhesion signaling and the transcriptional regulation of both stemness and immune escape. Collectively, these findings establish the dysadherin/YAP axis as a key driver of HCC progression and resistance, and highlight it as a compelling therapeutic target that could overcome treatment failure in advanced liver cancer.
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.