ArticleExperimental eye research2014
The clinically used photosensitizer Verteporfin (VP) inhibits YAP-TEAD and human retinoblastoma cell growth in vitro without light activation.
Article in Experimental eye research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers, 1 of them a synthesis that pooled it.
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
154 citing papers in PubMed, 1 synthesis or guideline pooled it, 221 citations in OpenAlex.
- The Hippo signalling pathway and its impact on eye diseases.Journal of cellular and molecular medicine · 2024Pooled it
- Cell differentiation-related signaling pathways: biological functions, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Reprogramming the Tumor Oncobiosphere: Bioactive Nanohybrid Materials for Reversing Therapeutic Pseudo-Resistance.ACS omega · 2026Review
- Beyond chemotherapy: the evolving role of photodynamic therapy in triple-negative breast cancer.Medical oncology (Northwood, London, England) · 2026Review
- Targeting stiffness-dependent YAP/TAZ restores angiogenesis dynamics impaired by ALK1 knockout in silico.PLoS computational biology · 2026Article
- Self-assembled verteporfin nanoparticles decrease drug efflux by P-glycoprotein without light activation in drug-resistant cancer cells.Bioengineering & translational medicine · 2026Article
- Mechanobiology of cancer-associated thrombosis: from molecular mechanisms to therapeutic innovation.Journal of nanobiotechnology · 2026Review
- The Hippo pathway in clear cell renal cell carcinoma (ccRCC): a nexus with the VHL disruption?Translational oncology · 2026Review
- Ambient light drives verteporfin-induced protein cross-linking during standard laboratory sample processing.PloS one · 2026Article
- Design and biological evaluation of peptide disruptors targeting YAP1-TEAD interaction for oral cancer.BMC oral health · 2025Article
- DysregulatedLife science alliance · 2025Article
- Review
- Hippo signaling pathway in human testis and seminoma: anticancer effect of verteporfin on human seminoma TCam-2 cells.Journal of molecular histology · 2025Article
- MST3 Regulates AMPK and YAP-Hippo Signaling in Cell Models Relevant to Renal Fibrosis.Biomolecules & therapeutics · 2025Article
- Pharmacological modulation of stem cells signaling pathway for therapeutic applications.Stem cell research & therapy · 2025Review
- Pannexin 1 crosstalk with the Hippo pathway in malignant melanoma.The FEBS journal · 2025Article
- Effects of Verteporfin on Interstitial Fluid Flow-Induced Fibrotic Transdifferentiation of Human Tenon Fibroblasts.Investigative ophthalmology & visual science · 2025Article
- Article
- A Theoretical Study on the Efficacy and Mechanism of Combined YAP-1 and PARP-1 Inhibitors in the Treatment of Glioblastoma Multiforme Using Peruvian MacaCurrent issues in molecular biology · 2025Article
- Recent advances on Hippo-YAP pathway in skin diseases.Frontiers in immunology · 2025Review
94 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Verteporfin (VP), a benzoporphyrin derivative, is clinically used in photodynamic therapy for neovascular macular degeneration. Recent studies indicate that VP may inhibit growth of hepatoma cells without photoactivation through inhibition of YAP-TEAD complex. In this study, we examined the effects of VP without light activation on human retinoblastoma cell lines. Verteporfin but not vehicle control inhibited the growth, proliferation and viability of human retinoblastoma cell lines (Y79 and WERI) in a dose-dependent manner and was associated with downregulation of YAP-TEAD associated downstream proto-oncogenes such as c-myc, Axl, and surviving. In addition VP affected signals involved in cell migration and angiogenesis such as CTGF, cyr61, and VEGF-A but was not associated with significant effect on the mTOR/autophagy pathway. Of interest the pluripotency marker Oct4 were downregulated by Verteporfin treatment. Our results indicate that the clinically used photosensitizer VP is a potent inhibitor of cell growth in retinoblastoma cells, disrupting YAP-TEAD signaling and pluripotential marker OCT4. This study highlights for the first time the role of the YAP-TEAD pathway in Retinoblastoma and suggests that VP may be a useful adjuvant therapeutic tool in treating Rb patients.
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.