ArticleCommunications biology2021
Fascin1 empowers YAP mechanotransduction and promotes cholangiocarcinoma development.
Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- FSCN1 induces subchondral bone sclerosis in osteoarthritis via modulating actin cytoskeleton dynamics and YAP signaling.Arthritis research & therapy · 2026Article
- Chick embryo extract-driven culture system enhances chicken muscle satellite cell differentiation and 3D myotube formation.NPJ science of food · 2025Article
- A Difluorinated Derivative of ARC-111 Suppresses Intrahepatic Cholangiocarcinoma Growth via Targeting Topoisomerase I.ACS pharmacology & translational science · 2025Article
- Mitochondrial mechanotransduction through MIEF1 coordinates the nuclear response to forces.Nature cell biology · 2024Article
- YAP/TAZ: Molecular pathway and disease therapy.MedComm · 2023Review
- Mechanical regulation of chromatin and transcription.Nature reviews. Genetics · 2022Review
- Lymphocyte-Specific Protein-1 Suppresses Xenobiotic-Induced Constitutive Androstane Receptor and Subsequent Yes-Associated Protein-Activated Hepatocyte Proliferation.The American journal of pathology · 2022Article
- Mitochondrial fission links ECM mechanotransduction to metabolic redox homeostasis and metastatic chemotherapy resistance.Nature cell biology · 2022Article
- Interplay Between Notch and YAP/TAZ Pathways in the Regulation of Cell Fate During Embryo Development.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Mechanical forces control cell behavior, including cancer progression. Cells sense forces through actomyosin to activate YAP. However, the regulators of F-actin dynamics playing relevant roles during mechanostransduction in vitro and in vivo remain poorly characterized. Here we identify the Fascin1 F-actin bundling protein as a factor that sustains YAP activation in response to ECM mechanical cues. This is conserved in the mouse liver, where Fascin1 regulates YAP-dependent phenotypes, and in human cholangiocarcinoma cell lines. Moreover, this is relevant for liver tumorigenesis, because Fascin1 is required in the AKT/NICD cholangiocarcinogenesis model and it is sufficient, together with AKT, to induce cholangiocellular lesions in mice, recapitulating genetic YAP requirements. In support of these findings, Fascin1 expression in human intrahepatic cholangiocarcinomas strongly correlates with poor patient prognosis. We propose that Fascin1 represents a pro-oncogenic mechanism that can be exploited during intrahepatic cholangiocarcinoma development to overcome a mechanical tumor-suppressive environment.
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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.