ArticleThe EMBO journal2018
YAP-TEAD signaling promotes basal cell carcinoma development via a c-JUN/AP1 axis.
Article in The EMBO journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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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.
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Who cites it
44 citing papers in PubMed, 75 citations in OpenAlex.
- Does Basal Cell Carcinoma Arise from a Precursor Lesion?The Journal of investigative dermatology · 2026Review
- KSR1 is a scaffold for the Hippo signaling pathway.Communications biology · 2025Article
- On the mechanisms of epidermal stemness and differentiation.NPJ systems biology and applications · 2025Article
- Double-sided niche regulation in skin stem cell and cancer: mechanisms and clinical applications.Molecular cancer · 2025Review
- Review
- circTP63-N suppresses the proliferation and metastasis of nasopharyngeal carcinoma via engaging with HSP90AB1 to modulate the YAP1/Hippo signaling pathway.Science China. Life sciences · 2025Article
- Ultraviolet B Exposure Does Not Influence the Expression of YAP mRNA in Human Epidermal Keratinocytes-Preliminary Study.Biomedicines · 2025Article
- Cooperation between the Hippo and MAPK pathway activation drives acquired resistance to TEAD inhibition.Nature communications · 2025Article
- Recent advances on Hippo-YAP pathway in skin diseases.Frontiers in immunology · 2025Review
- YAP/TAZ Signalling Controls Epidermal Keratinocyte Fate.International journal of molecular sciences · 2024Review
- A non-canonical repressor function of JUN restrains YAP activity and liver cancer growth.The EMBO journal · 2024Article
- Interplay between YAP/TAZ and metabolic dysfunction-associated steatotic liver disease progression.Archives of pharmacal research · 2024Review
- Article
- Spontaneously evolved progenitor niches escape Yap oncogene addiction in advanced pancreatic ductal adenocarcinomas.Nature communications · 2023Article
- YAP/TAZ as master regulators in cancer: modulation, function and therapeutic approaches.Nature cancer · 2023Review
- Targeting the Hippo/YAP/TAZ signalling pathway: Novel opportunities for therapeutic interventions into skin cancers.Experimental dermatology · 2022Review
- Decoding YAP dependent transcription in the liver.Nucleic acids research · 2022Article
- Review
- Basal cell carcinomas acquire secondary mutations to overcome dormancy and progress from microscopic to macroscopic disease.Cell reports · 2022Article
- Functional interaction between endothelin-1 and ZEB1/YAP signaling regulates cellular plasticity and metastasis in high-grade serous ovarian cancer.Journal of experimental & clinical cancer research : CR · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
The mammalian Hippo signaling pathway, through its effectors YAP and TAZ, coerces epithelial progenitor cell expansion for appropriate tissue development or regeneration upon damage. Its ability to drive rapid tissue growth explains why many oncogenic events frequently exploit this pathway to promote cancer phenotypes. Indeed, several tumor types including basal cell carcinoma (BCC) show genetic aberrations in the Hippo (or YAP/TAZ) regulators. Here, we uncover that while YAP is dispensable for homeostatic epidermal regeneration, it is required for BCC development. Our clonal analyses further demonstrate that the few emerging Yap-null dysplasia have lower fitness and thus are diminished as they progress to invasive BCC Mechanistically, YAP depletion in BCC tumors leads to effective impairment of the JNK-JUN signaling, a well-established tumor-driving cascade. Importantly, in this context, YAP does not influence canonical Wnt or Hedgehog signaling. Overall, we reveal Hippo signaling as an independent promoter of BCC pathogenesis and thereby a viable target for drug-resistant BCC.
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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.